604 results on '"Reckelhoff, Jane F."'
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2. Male Offspring Exposed to Maternal Hyperandrogenemia Have Exaggerated Pressor Response to Angiotensin II That Is Partially Attenuated by Etanercept
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Agbo, John, primary, Quin, Ruth, additional, Reckelhoff, Jane F., additional, and Shawky, Noha M., additional
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- 2024
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3. Consequences of hyperandrogenemia during pregnancy in female offspring: attenuated response to angiotensin II
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Shawky, Noha M., Dalmasso, Carolina, Ojeda, Norma B., Zuchowski, Yvonne, Stachenfeld, Nina, Alexander, Barbara T., and Reckelhoff, Jane F.
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- 2022
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4. Sex Differences in Regulation of Blood Pressure
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Reckelhoff, Jane F., COHEN, IRUN R., Series Editor, LAJTHA, ABEL, Series Editor, LAMBRIS, JOHN D., Series Editor, PAOLETTI, RODOLFO, Series Editor, REZAEI, NIMA, Series Editor, Kerkhof, Peter L. M., editor, and Miller, Virginia M., editor
- Published
- 2018
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- View/download PDF
5. List of Contributors
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Abramovitz, Blaise, primary, Adu, Dwomoa, additional, Afshinnia, Farsad, additional, Agarwal, Anupam, additional, Andrews, Sarah C., additional, Appel, Gerald, additional, Bailey, James L., additional, Bakris, George L., additional, Bauer, Carolyn A., additional, Baxi, Pravir V., additional, Berns, Jeffrey S., additional, Birks, Peter, additional, Bomback, Andrew, additional, Bose, Anirban, additional, Brosius, Frank C., additional, Brown, Lee K., additional, Bushinsky, David A., additional, Busse, Laurence W., additional, Campbell, Ruth C., additional, Canney, Mark, additional, Cathro, Helen, additional, Chávez-Iñiguez, Jonathan, additional, Chawla, Lakhmir S., additional, Chen, Sheldon, additional, Chertow, Glenn M., additional, Chew, Emily Y., additional, Chonchol, Michel, additional, Clegg, Deborah J., additional, Clive, David M., additional, Clive, Pia H., additional, Cohen, Scott D., additional, Collins, Ashte' K., additional, Cooper, James E., additional, Correa-Rotter, Ricardo, additional, Cukor, Daniel, additional, Dalal, Monica, additional, Davenport, Andrew, additional, Davis, Scott, additional, Davison, Sara N., additional, Delanaye, Pierre, additional, de Zeeuw, Dick, additional, Dobre, Mirela A., additional, Drawz, Paul, additional, Ebert, Natalie, additional, Eggers, Paul, additional, Ferrè, Silvia, additional, Freedman, Barry I., additional, Furth, Susan L., additional, Gao, Bixia, additional, García-García, Guillermo, additional, Gashti, Casey N., additional, Germino, Gregory G., additional, Goldsmith, David, additional, Golestaneh, Ladan, additional, Goligorsky, Michael S., additional, Greenberg, Arthur, additional, Gregg, L. Parker, additional, Guay-Woodford, Lisa M., additional, Hamm, Lee, additional, Hart, Allyson, additional, Haselby, Danielle, additional, Hedayati, S. Susan, additional, Heerspink, Hiddo J.L., additional, Herzog, Charles A., additional, Hostetter, Thomas H., additional, House, Andrew A., additional, Hruska, Keith A., additional, Ishani, Areef, additional, Isom, Robert T., additional, James, Matthew T., additional, Jhaveri, Kenar D., additional, Johansen, Kirsten, additional, Johnson, Richard J., additional, Kang, Duk-Hee, additional, Kanno, Hiroko, additional, Kanno, Yoshihiko, additional, Karambelkar, Amrita D., additional, Karet Frankl, Fiona E., additional, Khoury, Charbel C., additional, Kimmel, Paul L., additional, Kopp, Jeffrey B., additional, Korbet, Stephen M., additional, Kruzel-Davila, Etty, additional, Kummer, Andrew, additional, LaFave, Laura, additional, Lakkis, Jay I., additional, Lerman, Lilach O., additional, Levin, Adeera, additional, Lew, Susie Q., additional, Luyckx, Valerie A., additional, Mattoo, Tej K., additional, Maynard, Sharon E., additional, McCullough, Peter A., additional, Mehrotra, Rajnish, additional, Meyer, Timothy W., additional, Mitch, William E., additional, Moe, Orson W., additional, Mohandes, Samer, additional, Moss, Alvin H., additional, Moxey-Mims, Marva, additional, Murugapandian, Sangeetha, additional, Nath, Karl A., additional, Neugarten, Joel, additional, Neyra, Javier A., additional, Nissenson, Allen R., additional, Nobakht, Ehsan, additional, Nolin, Thomas D., additional, Norris, Keith C., additional, Norton, Jenna M., additional, Nowak, Kristen L., additional, Ojo, Akinlolu O., additional, Pahl, Madeleine V., additional, Paller, Mark S., additional, Palmer, Biff F., additional, Palmer, Nicholette D., additional, Patel, Samir S., additional, Pecoits-Filho, Roberto, additional, Peitzman, Steven J., additional, Peixoto, Aldo J., additional, Pham, Phuong-Thu T., additional, Pham, Phuong-Chi T., additional, Piraino, Beth, additional, Pisoni, Roberto, additional, Rabelink, Ton, additional, Radhakrishnan, Jai, additional, Rahman, Mahboob, additional, Raj, Dominic S., additional, Ramírez-Sandoval, Juan C., additional, Rangaswami, Janani, additional, Reckelhoff, Jane F., additional, Regunathan-Shenk, Renu, additional, Reule, Scott, additional, Ronco, Claudio, additional, Rosenberg, Mark E., additional, Rosner, Mitchell H., additional, Rovin, Brad, additional, Roy-Chaudhury, Prabir, additional, Ruebner, Rebecca, additional, Rule, Andrew D., additional, Sands, Jeff M., additional, Schlanger, Lynn E., additional, Schrauben, Sarah J., additional, Seliger, Stephen, additional, Shah, Maulin, additional, Sterns, Richard H., additional, Stites, Erik, additional, Sugatani, Toshifumi, additional, Textor, Stephen C., additional, Thadhani, Ravi, additional, Thajudeen, Bijin, additional, Thakar, Surabhi, additional, Thomas, George, additional, Townsend, Raymond R., additional, Turner, Jeffrey, additional, Unruh, Mark L., additional, Urquhart, Bradley L., additional, Vassalotti, Joseph A., additional, Vaziri, Nosratola D., additional, Velasquez, Manuel T., additional, Ver Halen, Nisha, additional, Waddy, Salina P., additional, Wang, Jinwei, additional, Weber, Marc, additional, Weir, Matthew R., additional, White, Christine A., additional, Whittier, William L., additional, Williams, Matthew J., additional, Wiseman, Alexander C., additional, Wymer, David C., additional, Wymer, David T.G., additional, Yee, Jerry, additional, Zhang, Luxia, additional, Zhuang, Shougang, additional, and Ziyadeh, Fuad N., additional
- Published
- 2020
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6. Gender Issues in Chronic Kidney Disease
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Neugarten, Joel, primary and Reckelhoff, Jane F., additional
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- 2020
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7. Connecting Generations of Scientists in the Council on Hypertension Through Harriet Dustan
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Watts, Stephanie W., Alexander, Barbara T., Baylis, Chris, Brown, Nancy J., Cassis, Lisa A., Denton, Kate M., Joe, Bina, Lerman, Lilach O., Oparil, Suzanne, Reckelhoff, Jane F., Sandberg, Kathryn, and Touyz, Rhian M.
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- 2021
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8. Testosterone-associated blood pressure dysregulation in women with androgen excess polycystic ovary syndrome
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Stone, Tori, primary, Yanes Cardozo, Licy L., additional, Oluwatade, Toni N., additional, Leone, Cheryl A., additional, Burgos, Melanie, additional, Okifo, Faith, additional, Pal, Lubna, additional, Reckelhoff, Jane F., additional, and Stachenfeld, Nina. S., additional
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- 2023
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9. Insights Into the Cardiomodulatory Effects of Sex Hormones: Implications in Transgender Care
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Shawky, Noha M., primary, Reckelhoff, Jane F., additional, Alexander, Barbara T., additional, and Yanes Cardozo, Licy L., additional
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- 2023
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10. Contributors
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AlSiraj, Yasir, primary, Baker, Sarah E., additional, Barcena, Maria Louisa, additional, Barsha, Giannie, additional, Bean, Cynthia, additional, Bourque, Stephane L., additional, Brooks, Heddwen L., additional, Cassis, Lisa A., additional, Cornelius, Denise C., additional, Davidge, Sandra T., additional, Davis, Melinda B., additional, den Ruijter, Hester, additional, Denton, Kate M., additional, Duvernoy, Claire S., additional, Eikendal, Anouk, additional, Garnier, Anne, additional, Garovic, Vesna D., additional, Goulopoulou, Styliani, additional, Harbuz-Miller, Inga, additional, Harris, Sharonda, additional, Hartman, Robin, additional, Hay, Meredith, additional, Husband, Nathaniel, additional, Johnson, Alan Kim, additional, Joyner, Michael, additional, Kattah, Andrea G., additional, Kawamoto, Kris, additional, Kwok, Edmund, additional, Lastra, Guido, additional, Limberg, Jacqueline K., additional, Loria, Analia S., additional, Manrique, Camila M., additional, Martin, James N., additional, Mathis, Keisa W., additional, McCullough, Louise D., additional, Morgentaler, Abraham, additional, Morris, Rachael F., additional, Pham, Quin, additional, Pham, Grace S., additional, Pollow, Dennis P., additional, Poudel, Bibek, additional, Ranadive, Sushant M., additional, Reckelhoff, Jane F., additional, Regitz-Zagrosek, Vera, additional, Romero, Damian G., additional, Roy-O’Reilly, Meaghan, additional, Samson, Willis K., additional, Shields, Corbin A., additional, Sowers, James R., additional, Thatcher, Sean E., additional, Torres Fernandez, Edgar D., additional, Traish, Abdulmaged M., additional, Uhlorn, Josh, additional, Ventura-Clapier, Renee, additional, Wallace, Kedra, additional, Walton, Sarah L., additional, Williams, Jan Michael, additional, Woolley, Cassandra, additional, Xue, Baojian, additional, Yanes Cardozo, Licy L., additional, and Yosten, Gina L.C., additional
- Published
- 2019
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11. Androgens and Cardiovascular Diseases in Women
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Yanes Cardozo, Licy L., primary, Torres Fernandez, Edgar D., additional, Romero, Damian G., additional, and Reckelhoff, Jane F., additional
- Published
- 2019
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12. Pregnancy Protects Hyperandrogenemic Female Rats From Postmenopausal Hypertension
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Shawky, Noha M., Patil, Chetan N., Dalmasso, Carolina, Maranon, Rodrigo O., Romero, Damian G., Drummond, Heather, and Reckelhoff, Jane F.
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- 2020
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13. Is My Study Sex or Is it Gender?
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Reckelhoff, Jane F., primary
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- 2023
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14. Human Umbilical Venous Endothelial Cells: Early Predictors of Cardiovascular Risk in Offspring?: What Is Known and What More Needs to Be Investigated?
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Reckelhoff, Jane F., LaMarca, Babbette, Garovic, Vesna D., and Alexander, Barbara T.
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- 2019
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15. Animal Models of Hypertension: A Scientific Statement From the American Heart Association
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Lerman, Lilach O., Kurtz, Theodore W., Touyz, Rhian M., Ellison, David H., Chade, Alejandro R., Crowley, Steven D., Mattson, David L., Mullins, John J., Osborn, Jeffrey, Eirin, Alfonso, Reckelhoff, Jane F., Iadecola, Costantino, and Coffman, Thomas M.
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- 2019
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16. Models of Hypertension in Aging
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Reckelhoff, Jane F., primary, Yanes Cardozo, Licy L., additional, and Fortepiani, Maria Lourdes Alarcon, additional
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- 2018
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17. List of Contributors
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Abdel-Rahman, Emaad M., primary, Ackerman, Hayley D., additional, Akintola, Abimbola, additional, Amdam, Gro V., additional, Atzmon, Gil, additional, Austad, Steve, additional, Awate, Sanket, additional, Balaskó, Márta, additional, Banerjee, Taraswi, additional, Bárcena, Clea, additional, Bartke, Andrzej, additional, Bassi, Ivan, additional, Berendt, Mette, additional, Bijlsma, Maarten F., additional, Bitto, Alessandro, additional, Bizon, Jennifer L., additional, Bollaerts, Ilse, additional, Bonomi, Marco, additional, Borras, Consuelo, additional, Bowman, Brendan T., additional, Brioche, Thomas, additional, Brosh, Robert M., additional, Brown, Richard E., additional, Buck, Kerstin, additional, Burke, Sara N., additional, Buzgariu, Wanda, additional, Cacabelos, Ramón, additional, Camina Martín, M.A., additional, Chaffee, Beth K., additional, Chan, Anthony W.S., additional, Chen, Haolin, additional, Chen, Zhiguo, additional, Cho, In K., additional, Chopard, Angèle, additional, Cogger, Victoria C., additional, Cohen, Alan A., additional, Confino, Rafael, additional, Coppedè, Fabio, additional, Costa, Anthony J., additional, Crouch, Jack D., additional, Darcy, Justin, additional, De Groef, Lies, additional, de Mateo Silleras, B., additional, Deepa, Sathyaseelan S., additional, Devau, Gina, additional, Dhenain, Marc, additional, Dills, Chantelle, additional, Duffy, Megan F., additional, Duncan, Francesca E., additional, Dupuis, Gilles, additional, Eaton, Benjamin A., additional, Egan, Josephine M., additional, Ekundayo, Kazadi, additional, Emborg, Marina E., additional, Fischer, D. Luke, additional, Fontes, Pascaline, additional, Fortepiani, Maria Lourdes Alarcon, additional, Fortin, Carl, additional, Franzke, Bernhard, additional, Fülöp, Tamas, additional, Gabriel, Camelia, additional, Galliot, Brigitte, additional, Gambini, Juan, additional, Garneau, Hugo, additional, Gasparini, Laura, additional, Gerhard, Glenn S., additional, Gibson, David C., additional, Gimeno-Mallench, Lucia, additional, Girard, Victor, additional, Greer, Kimberly A., additional, Gribble, Kristin E., additional, Gubbels Bupp, Melanie R., additional, Gudmundsson, Adalsteinn, additional, Hamann, Andrea, additional, Hamblin, Michael R., additional, Harper, James M., additional, Hart, Ronald, additional, Head, Elizabeth, additional, Herd, Heather R., additional, Herrera, Guadalupe, additional, Hisama, Fuki M., additional, Hogan, David B., additional, Holmes, Donna J., additional, Hornsby, Peter J., additional, Howlett, Susan E., additional, Hui, Ka Yi, additional, Jahn, Thomas R., additional, Jávega, Beatriz, additional, Jeffery, William R., additional, Johnson, Sarah A., additional, Jones, Audrey, additional, Jones, Corinne A., additional, Jónsson, Pálmi V., additional, Kane, Alice E., additional, Karasik, David, additional, Kean, Samuel, additional, Keller, Evan T., additional, Keller, Jill M., additional, Kemp, Christopher J., additional, Wong, Ken S.K., additional, Krøll, Jens, additional, Kumar Bharti, Sanjay, additional, Kurkinen, Markku, additional, Larbi, Anis, additional, Lasbleiz, Christelle, additional, Lautier, Corinne, additional, Le Couteur, David G., additional, Le Page, Aurelie, additional, Lin, Hang, additional, López-Otín, Carlos, additional, Lottonen-Raikaslehto, Line, additional, Magden, Elizabeth R., additional, Makrantonaki, Evgenia, additional, Manfredsson, Fredric P., additional, Mark Welch, David B., additional, Marques-Lopes, Jose, additional, Martínez-Romero, Alicia, additional, Mas-Bargues, Cristina, additional, Mayoral, Pablo, additional, Mc Auley, Mark, additional, McQuail, Joseph A., additional, Merentie, Mari, additional, Mestre-Frances, Nadine, additional, Metzger, Jeanette M., additional, Meyer, Keith C., additional, Milner, Teresa A., additional, Mizutani, Claudia M., additional, Monnat, Raymond J., additional, Mooney, Kathleen, additional, Moons, Lieve, additional, Muck, Joscha, additional, Muniyappa, Ranganath, additional, Nehlin, Jan O., additional, Neubauer, Oliver, additional, Nikolakis, Georgios, additional, Nyman, Jeffry S., additional, O’Connor, José-Enrique, additional, Oshima, Junko, additional, Osiewacz, Heinz D., additional, Papadopoulos, Vassilios, additional, Pavone, Mary Ellen, additional, Pawelec, Graham, additional, Pedersen, Jan T., additional, Perez-Lopez, Gonzalo, additional, Persani, Luca, additional, Pétervári, Erika, additional, Peyman, Azadeh, additional, Plate, Johannes F., additional, Polinski, Nicole K., additional, Py, Guillaume, additional, Quigley, Tyler P., additional, Rae, Eric A., additional, Ram, Jeffrey L., additional, Raubenheimer, David, additional, Reckelhoff, Jane F., additional, Redondo del Río, M.P., additional, Rex-Al Panem Orbon, Jovy, additional, Richardson, Arlan, additional, Ripperger, Jürgen A., additional, Rostás, Ildikó, additional, Rouse, Michael, additional, Rueppell, Olav, additional, Runge, Kurt W., additional, Safdar, Maryam, additional, Sankaran-Walters, Sumathi, additional, Santago, Anthony C., additional, Sarvimäki, Anneli, additional, Saul, Katherine R., additional, Schenkelaars, Quentin, additional, Schneider, Brandt L., additional, Schütt, Trine, additional, Shen, He, additional, Shin, Sooyoun, additional, Simpson, Stephen J., additional, Smith, Jessica, additional, Snell, Terry W., additional, Snyder, Jessica M., additional, Solon-Biet, Samantha M., additional, Soós, Szilvia, additional, Sortwell, Caryl E., additional, Sousa-Neves, Rui, additional, Steece-Collier, Kathy, additional, Steins, Anne, additional, Sujkowski, Alyson, additional, Swanberg, Susan E., additional, Teijido, Oscar, additional, Tella, Sri Harsha, additional, Tenk, Judit, additional, Tomczyk, Szymon, additional, Treuting, Piper M., additional, Trouche, Stéphanie G., additional, Tuan, Rocky S., additional, Unnikrishnan, Archana, additional, Valenzano, Dario Riccardo, additional, van Heemst, Diana, additional, Van houcke, Jessie, additional, Van Kempen, Tracey A., additional, van Laarhoven, Hanneke W.M., additional, Verdier, Jean-Michel, additional, Viña, Jose, additional, Wagner, Karl-Heinz, additional, Wahl, Devin, additional, Wenger, Yvan, additional, Wessells, Robert J., additional, Wilcock, Donna M., additional, Witkowski, Jacek M., additional, Wong, Esther, additional, Woodland, Nicole, additional, Yanes Cardozo, Licy L., additional, Ylä-Herttuala, Seppo, additional, Youssef, Sameh A., additional, Yuan, Rong, additional, Zhang, Haitao, additional, Zhou, Zhongjun, additional, Zirkin, Barry R., additional, and Zouboulis, Christos C., additional
- Published
- 2018
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18. PS-B06-3: SEX-SPECIFIC EFFECTS OF IMMUNOSUPPRESSANTS ON SPONTANEOUSLY HYPERTENSIVE RATS
- Author
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Maranon, Rodrigo O, primary, Reckelhoff, Jane F, additional, and Moulana, Mohadetheh, additional
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- 2023
- Full Text
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19. Role of Oxidative Stress in Mediating Elevated Blood Pressure with Aging
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Valinotti, Julio Sartori, Yanes, Licy, Reckelhoff, Jane F., Bondy, Stephen, editor, and Maiese, Kenneth, editor
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- 2010
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- View/download PDF
20. Polycystic Ovary Syndrome: Insights from Preclinical Research
- Author
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Reckelhoff, Jane F., primary, Shawky, Noha M., additional, Romero, Damian G., additional, and Yanes Cardozo, Licy L., additional
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- 2022
- Full Text
- View/download PDF
21. The Vasodilatory Effect of Testosterone on Renal Afferent Arterioles
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Lu, Yan, Fu, Yiling, Ge, Ying, Juncos, Luis A., Reckelhoff, Jane F., and Liu, Ruisheng
- Published
- 2012
- Full Text
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22. Post‐Pubertal Testosterone Implants Induce Hypertension in Female‐to‐Male Trans‐Sex Rat Model
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Shawky, Noha M., primary, Yanes Cardozo, Licy, additional, and Reckelhoff, Jane F., additional
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- 2022
- Full Text
- View/download PDF
23. Administration of Estradiol in Young Adulthood in the Male Sprague Dawley Rat to Mimic Female Physiological Levels is Associated with a Reduction in Body Weight, Lean Mass and Testicular Size
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Alexander, Barbara T., primary, Rawls, Adam Z., additional, Cockrell, Kathy, additional, Davenport, Kacey, additional, Ojeda, Norma B., additional, Reckelhoff, Jane F., additional, Yanes Cardozo, Licy L., additional, and Shawky, Noha M., additional
- Published
- 2022
- Full Text
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24. Cardiovascular-Renal and Metabolic Characterization of a Rat Model of Polycystic Ovary Syndrome
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Yanes, Licy L., Romero, Damian G., Moulana, Mohaddetheh, Lima, Roberta, Davis, Deborah D., Zhang, Huimin, Lockhart, Rachel, Racusen, Lorraine C., and Reckelhoff, Jane F.
- Published
- 2011
- Full Text
- View/download PDF
25. List of Contributors
- Author
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Afshinnia, Farsad, primary, Agarwal, Anupam, additional, Appel, Gerald B., additional, Bagby, Susan P., additional, Bailey, James L., additional, Bakris, George L., additional, Barrett, Brendan J., additional, Bauer, Carolyn A., additional, Berl, Tomas, additional, Berns, Jeffrey S., additional, Bomback, Andrew, additional, Bose, Anirban, additional, Brosius, Frank C., additional, Brown, Lee K., additional, Bushinsky, David A., additional, Busse, Laurence W., additional, Campbell, Ruth C., additional, Cathro, Helen, additional, Chawla, Lakhmir S., additional, Chen, Sheldon, additional, Chertow, Glenn M., additional, Chew, Emily, additional, Chonchol, Michel, additional, Clive, David M., additional, Cohen, Debbie L., additional, Cohen, Lewis M., additional, Cohen, Scott D., additional, Collins, Ashte’ K., additional, Combs, Sara, additional, Correa-Rotter, Ricardo, additional, Cukor, Daniel, additional, Dalal, Monica, additional, Dancik, Tavis, additional, Davenport, Andrew, additional, Davison, Sara, additional, Zeeuw, Dick de, additional, Delanaye, Pierre, additional, Dharia, Sushma M., additional, Dobre, Mirela A., additional, Drawz, Paul, additional, Dreisbach, Albert W., additional, Emmett, Michael, additional, Fanton, John H., additional, Felsenfeld, Arnold J., additional, Fernandez, Hilda, additional, Flessner, Michael F., additional, Freedman, Barry I., additional, Fruchter, Yvette, additional, Furth, Susan L., additional, García-García, Guillermo, additional, Germain, Michael J., additional, Germino, Gregory G., additional, Goligorsky, Michael S., additional, Greenberg, Arthur, additional, Guay-Woodford, Lisa M., additional, Hawkins, Katrina, additional, Herzog, Charles A., additional, Holley, Jean L., additional, Hostetter, Thomas H., additional, House, Andrew A., additional, Hruska, Keith A., additional, Huan, Yonghong, additional, Ibrahim, Hassan N., additional, Imran, Nashat, additional, Iñiguez, Jonathan Chávez, additional, Isom, Robert T., additional, Jablonski, Kristen L., additional, Jhaveri, Kenar D., additional, Johansen, Kirsten, additional, Johnson, Richard J., additional, Junghare, Milind Y., additional, Kang, Duk-Hee, additional, Karadsheh, Feras F., additional, Kari, Jameela, additional, Kasiske, Bertram L., additional, Khoury, Charbel C., additional, Kimmel, Paul L., additional, Kopp, Jeffrey B., additional, Kummer, Andrew, additional, Heerspink, Hiddo J.Lambers, additional, Lerman, Lilach O., additional, Levin, Adeera, additional, Levine, Barton S., additional, Lew, Susie Q., additional, Mandayam, Sreedhar, additional, Mattoo, Tej K., additional, Maynard, Sharon E., additional, Meyer, Timothy W., additional, Mitch, William E., additional, Moss, Alvin H., additional, Moxey-Mims, Marva, additional, Muntner, Paul, additional, Murray, Anne M., additional, Nath, Karl A., additional, Neugarten, Joel, additional, No, Gloria, additional, Pahl, Madeleine V., additional, Paller, Mark S., additional, Palmer, Biff F., additional, Parfrey, Patrick S., additional, Patel, Samir S., additional, Pecoits-Filho, Roberto, additional, Peitzman, Steven J., additional, Peixoto, Aldo J., additional, Pham, Phuong-Chi T., additional, Pham, Phuong-Thu T., additional, Rabelink, Ton J., additional, Radhakrishnan, Jai, additional, Raed, Anas, additional, Raj, Dominic S., additional, Ramirez-Sandoval, Juan Carlos, additional, Reckelhoff, Jane F., additional, Ronco, Claudio, additional, Rosenberg, Mark E., additional, Rosner, Mitchell H., additional, Rovin, Brad, additional, Roy-Chaudhury, Prabir, additional, Ruebner, Rebecca, additional, Rule, Andrew D., additional, Sands, Jeff M., additional, Scheinman, Steven J., additional, Schlanger, Lynn E., additional, Seifert, Michael E., additional, Seliger, Stephen, additional, Singh, Ajay K., additional, Stendahl, John C., additional, Surendran, Kameswaran, additional, Textor, Stephen C., additional, Thadhani, Ravi I., additional, Townsend, Raymond R., additional, Unruh, Mark L., additional, Vassalotti, Joseph A., additional, Vaziri, Nosratola D., additional, Velasquez, Manuel T., additional, Ver Halen, Nisha, additional, Wang, Connie J., additional, Wanner, Christoph, additional, Weber, Marc, additional, Weir, Matthew R., additional, Wing, Maria R., additional, Winn, Michelle P., additional, Wymer, David C., additional, Yee, Jerry, additional, and Ziyadeh, Fuad N., additional
- Published
- 2015
- Full Text
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26. Gender Issues in Chronic Kidney Disease
- Author
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Neugarten, Joel, primary and Reckelhoff, Jane F., additional
- Published
- 2015
- Full Text
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27. Abstract P184: Aging Male Offspring Of Polycystic Ovary Syndrome Rat Model Have Normal Blood Pressure And Exaggerated Pressor Response To Angiotensin II
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Shawky, Noha M, primary and Reckelhoff, Jane F, additional
- Published
- 2021
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- View/download PDF
28. Mep-1 Gene Controlling a Kidney Metalloendopeptidase is Linked to the Major Histocompatibility Complex in Mice
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Bond, Judith S., Beynon, Robert J., Reckelhoff, Jane F., and David, Chella S.
- Published
- 1984
29. Cardiometabolic consequences of maternal hyperandrogenemia in male offspring
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Zuchowski, Yvonne, primary, Dalmasso, Carolina, additional, Shawky, Noha M., additional, and Reckelhoff, Jane F., additional
- Published
- 2021
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- View/download PDF
30. Hypertension in Postmenopausal Women
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Lima, Roberta, Wofford, Marion, and Reckelhoff, Jane F.
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- 2012
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31. Metabolic Syndrome, Androgens, and Hypertension
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Moulana, Mohadetheh, Lima, Roberta, and Reckelhoff, Jane F.
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- 2011
- Full Text
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32. Chapter 7 - Gender Issues in Chronic Kidney Disease
- Author
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Neugarten, Joel and Reckelhoff, Jane F.
- Published
- 2020
- Full Text
- View/download PDF
33. Testosterone-dependent hypertension and upregulation of intrarenal angiotensinogen in Dahl salt-sensitive rats
- Author
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Yanes, Licy L., Sartori-Valinotti, Julio C., Iliescu, Radu, Romero, Damian G., Racusen, Lorraine C., Zhang, Huimin, and Reckelhoff, Jane F.
- Subjects
Hypertension -- Risk factors ,Hypertension -- Genetic aspects ,Hypertension -- Research ,Kidney diseases -- Risk factors ,Kidney diseases -- Genetic aspects ,Kidney diseases -- Research ,Renin-angiotensin system -- Physiological aspects ,Renin-angiotensin system -- Research ,Testosterone -- Health aspects ,Testosterone -- Research ,Biological sciences - Abstract
Blood pressure (BP) is more salt sensitive in men than in premenopausal women. In Dahl salt-sensitive rats (DS), high-salt (HS) diet increases BP more in males than females. In contrast to the systemic renin-angiotensin system, which is suppressed in response to HS in male DS, intrarenal angiotensinogen expression is increased, and intrarenal levels of ANG II are not suppressed. In this study, the hypothesis was tested that there is a sexual dimorphism in HS-induced upregulation of intrarenal angiotensinogen mediated by testosterone that also causes increases in BP and renal injury. On a low-salt (LS) diet, male DS had higher levels of intrarenal angiotensinogen mRNA than females. HS diet for 4 wk increased renal cortical angiotensinogen mRNA and protein only in male DS, which was prevented by castration. Ovariectomy of female DS had no effect on intrarenal angiotensinogen expression on either diet. Radiotelemetric BP was similar between males and castrated rats on LS diet. HS diet for 4 wk caused a progressive increase in BP, protein and albumin excretion, and glomerular sclerosis in male DS rats, which were attenuated by castration. Testosterone replacement in castrated DS rats increased BP, renal injury, and upregulation of renal angiotensinogen associated with HS diet. Testosterone contributes to the development of hypertension and renal injury in male DS rats on HS diet possibly through upregulation of the intrarenal renin-angiotensin system. androgens; hypertension; renal injury; glomerular sclerosis; angiotensinogen
- Published
- 2009
34. Rosiglitazone decreases blood pressure and renal injury in a female mouse model of systemic lupus erythematosus
- Author
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Venegas-Pont, Marcia, Sartori-Valinotti, Julio C., Maric, Christine, Racusen, Lorraine C., Glover, Porter H., McLemore, Gerald R., Jr., Jones, Allison V., Reckelhoff, Jane F., and Ryan, Michael J.
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Hypertension -- Risk factors ,Hypertension -- Drug therapy ,Hypertension -- Research ,Kidney diseases -- Risk factors ,Kidney diseases -- Drug therapy ,Kidney diseases -- Research ,Rosiglitazone maleate -- Dosage and administration ,Rosiglitazone maleate -- Research ,Systemic lupus erythematosus -- Complications and side effects ,Systemic lupus erythematosus -- Research ,Biological sciences - Abstract
Women with systemic lupus erythematosus (SLE) exhibit a high prevalence of hypertension and renal injury. Rosiglitazone (Rosi), a peroxisome proliferator activator receptor gamma ([PPAR.sub.[gamma]]) agonist, has renal protective and antihypertensive effects. We tested whether Rosi ameliorates hypertension and renal injury in a female mouse model of SLE (NZBWF1). Thirty-week-old SLE and control (NZW/LacJ) mice (n [greater than or equal to] 6/group) were fed Rosi (5 mg x [kg.sup.-1] x [day.sup.-1] in standard chow) or standard chow for 4 wk. SLE mice had increased blood pressure (BP in mmHg) compared with controls (139 [+ or -] 4 vs. 111 [+ or -] 4, P < 0.05). Rosi treatment lowered BP in SLE mice (127 [+ or -] 4, P < 0.05) but not in controls (111 [+ or -] 4). Urinary albumin ([micro]g/mg creatinine) was increased in SLE mice compared with controls (12,396 [+ or -] 6,525 vs. 50 [+ or -] 6) and reduced with Rosi treatment (148 [+ or -] 117). Glomerulosclerosis (% of glomeruli with sclerosis) was reduced in Rosi-treated SLE mice (4.2 [+ or -] 1.6 vs. 0.4 [+ or -] 0.3, P < 0.05). Renal monocyte/ macrophage numbers (cell number/1,320 points counted) were reduced in SLE mice treated with Rosi (32.6 [+ or -] 11.0 vs. 10.6 [+ or -] 3.6, P < 0.05) but unchanged in controls (3.7 [+ or -] 1.6 vs. 3.7 [+ or -] 2.0). Renal osteopontin expression, a cytokine-regulating macrophage recruitment, was reduced in Rosi-treated SLE mice. Urinary endothelin (in pg/mg creatinine) was increased in SLE mice compared with controls (1.9 [+ or -] 0.59 vs. 0.6 [+ or -] 0.04, P < 0.05) and reduced in SLE mice treated with Rosi (0.8 [+ or -] 0.11, P < 0.05). [PPAR.sup.[gamma]]/protein expression in the renal cortex was significantly lower in SLE mice compared with controls and was unaffected by Rosi. These data suggest that Rosi may be an important therapeutic option for the treatment of SLE hypertension and renal injury. lupus; inflammation; endothelin; glomerulosclerosis; proliferator activated receptor gamma
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- 2009
35. Sex differences in control of blood pressure: role of oxidative stress in hypertension in females
- Author
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Lopez-Ruiz, Arnaldo, Sartori-Valinotti, Julio, Yanes, Licy L., Iliescu, Radu, and Reckelhoff, Jane F.
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Oxidative stress -- Influence ,Hypertension -- Development and progression ,Hypertension -- Demographic aspects ,Blood pressure -- Measurement ,Biological sciences - Abstract
In general, blood pressure is higher in normotensive men than in age-matched women, and the prevalence of hypertension in men is also higher until after menopause, when the prevalence of hypertension increases for women. It is likely then that the mechanisms by which blood pressure increases in men and women with aging may be different. Although clinical trials to reduce blood pressure with antioxidants have typically not been successful in human cohorts, studies in male rats suggest that oxidative stress plays an important role in mediating hypertension. The exact mechanisms by which oxidative stress increases blood pressure have not been completely elucidated. There may be several reasons for the discrepancies between clinical and animal studies. In this review, the data obtained in selected clinical and animal studies are discussed, and the hypothesis is put forward that oxidative stress may not be as important in mediating hypertension in females as has been shown previously in male rats. Furthermore, it is likely that differences in genetics, age, length of time with hypertension, endothelial dysfunction, and sex are all factored in to modulate the responses to antioxidants in humans. As such, future clinical trials should be designed and powered to evaluate the effects of oxidative stress on blood pressure separately in men and women. [F.sub.2]-isoprostanes
- Published
- 2008
36. HO-1 induction lowers blood pressure and superoxide production in the renal medulla of angiotensin II hypertensive mice
- Author
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Vera, Trinity, Kelsen, Silvia, Yanes, Licy L., Reckelhoff, Jane F., and Stec, David E.
- Subjects
Angiotensin -- Analysis ,Hypertension -- Care and treatment ,Biological sciences - Abstract
Heme oxygenase-1 (HO-1) induction can attenuate the development of angiotensin II (ANG II)-dependent hypertension. However, the mechanism by which HO-1 lowers blood pressure in this model is not clear. The goal of this study was to test the hypothesis that induction of HO-1 in the kidney can attenuate the increase in reactive oxygen species (ROS) generation in the kidney that occurs during ANG II-dependent hypertension. Mice were divided into four groups, control (Con), cobalt protoporphyrin (CoPP), ANG II, and ANG II + CoPP. CoPP treatment (50 mg/kg) was administered in a single subcutaneous injection 2 days prior to implantation of an osmotic minipump that infused ANG II at a rate of 1 [micro]g*[kg.sub.-1]*[min.sup.-1]. At the end of this period, mean arterial blood pressure (MAP) averaged 93 [+ or -] 5, 90 [+ or -] 5, 146 [+ or -] 8, and 105 [+ or -] 6 mmHg in Con, CoPP-, ANG II-, and ANG II + CoPP-treated mice. To determine whether HO-1 induction resulted in a decrease in ANG H-stimulated ROS generation in the renal medulla, superoxide production was measured. Medullary superoxide production was increased by ANG II infusion and normalized in mice pretreated with CoPP. The reduction in ANG II-mediated superoxide production in the medulla with CoPP was associated with a decrease in extracellular superoxide dismutase protein but an increase in catalase protein and activity. These results suggest that reduction in superoxide and possibly hydrogen peroxide production in the renal medulla may be a potential mechanism by which induction of HO-1 with CoPP lowers blood pressure in ANG-II dependent hypertension. kidney; reactive oxygen species; cobalt protoporphyrin
- Published
- 2007
37. Impact of androgen-induced oxidative stress on hypertension in male SHR
- Author
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Iliescu, Radu, Cucchiarelli, Valeria E., Yanes, Licy L., Iles, Joshua W., and Reckelhoff, Jane F.
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Oxidative stress -- Research ,Androgens -- Research ,Superoxide -- Structure ,Superoxide -- Research ,Hypertension -- Research ,Biological sciences - Abstract
Men have higher blood pressure than women, and androgens and oxidative stress have been implicated as playing roles in this sexual dimorphism. The spontaneously hypertensive rat (SHR) is an animal model of both androgen- and oxidative stress-mediated hypertension. Therefore, the present studies were performed to test the hypothesis that androgens cause hypertension in SHR in part by stimulating superoxide production via NADPH oxidase. Castration of male SHR reduced blood pressure by 15% and attenuated both basal and NADPH-stimulated superoxide production in kidney cortical homogenates. Expression of [p47.sup.phox] and [gp91.sup.phox] but not [p22.sup.phox] subunits of NADPH oxidase were significantly lower in kidney cortex from castrated males compared with intact males. Moreover, inhibition of NADPH oxidase with apocynin caused ~15 mmHg reduction in blood pressure and reduced basal and NADPH-stimulated superoxide production in intact male SHR, but had no effect on blood pressure or superoxide production in castrated males. These data support the hypothesis that androgens cause oxidative stress and thereby increase blood pressure in male SHR via an NADPH oxidase-dependent mechanism. hypertension; oxidative stress; androgens; superoxide anion; spontaneously hypertensive rat
- Published
- 2007
38. Hypertension in Women
- Author
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Reckelhoff, Jane F., primary and Wofford, Marion, additional
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- 2013
- Full Text
- View/download PDF
39. List of Contributors
- Author
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Abusief, Mary E., primary, Acevedo-Garcia, Dolores, additional, Albert, Christine, additional, Lee Alekel, D., additional, Alemany, Laia, additional, Allen, Kelli D., additional, Anderson, Lauren M., additional, Apelberg, Benjamin J., additional, Atrash, Hani K., additional, Baird, Donna Day, additional, Merz, Noel Bairey C., additional, Baldwin, Carol M., additional, Barbieri, Robert L., additional, Baron, Shirley R., additional, Bassuk, Shari S., additional, Bates, Lisa M., additional, Beasley, Jeannette M., additional, Bell, Iris R., additional, Bergeman, C.S., additional, Berkman, Lisa F., additional, Bernstein, Jonine L., additional, Bernstein, Leslie, additional, Bertone-Johnson, Elizabeth R., additional, Beth Thomeer, Mieke, additional, Bisconti, Toni L., additional, Blair, Janet, additional, Bonifas, Robin P., additional, Bosch, Xavier F., additional, Bradford, Judith, additional, Bray, Freddie, additional, Brooks, Jennifer D., additional, Bromberger, Joyce, additional, Brown, Joelle M., additional, Bruni, Laia, additional, Bulik, Cynthia M., additional, Burkman, Ronald T., additional, Burstein, Marcy, additional, Bushnell, Cheryl, additional, Buss, Mary K., additional, Cauley, Jane A., additional, Celum, Connie L., additional, Chen, Xinhua, additional, Chevarie-Davis, Myriam, additional, Chiuve, Stephanie, additional, Chocano-Bedoya, Patricia O., additional, Chowdhary, Harjinder, additional, Christiani, David C., additional, Chung, Nadia T., additional, Clancy, Carolyn M., additional, Clark, Cari Jo, additional, Conen, David, additional, Costenbader, K.H., additional, Devlin, Amy, additional, Diaz, Mireia, additional, Douwes, Jeroen, additional, Drangsholt, Mark, additional, Driscoll, Ira, additional, DuBeau, Catherine E., additional, Edwards, Emmeline, additional, Ehrenstein, Vera, additional, Escalante, Agustín, additional, Espeland, Mark A., additional, Fitzgerald, Kathryn C., additional, Foxman, Betsy, additional, Franco, Eduardo, additional, Fraser, William D., additional, Fredriksen-Goldsen, Karen I., additional, Freeman, Ellen E., additional, Friesen, Melissa C., additional, Gadermann, Anne M., additional, Gaudet, Mia M., additional, Gavrilidis, Emmy, additional, Gaydos, Charlotte A, additional, Geronimo, Kimberly, additional, Geronimus, Arline T., additional, Gillespie, Robin Mary, additional, Giovannucci, Edward, additional, Glanz, Karen, additional, Glynn, Robert J., additional, Gold, Ellen, additional, Goldfarb, Shari, additional, Goldman, Marlene B., additional, Gower, Emily W., additional, Grainger, David A., additional, Green, Adèle C., additional, Haggerty, Catherine L., additional, Hardy, Rebecca, additional, Harlow, Bernard L., additional, Harlow, Siobán D., additional, Hartge, Patricia, additional, Haskin, Christine, additional, Herbert, Robin, additional, Holt, Victoria L., additional, Hoover, Robert N., additional, Houtchens, Maria K., additional, Husten, Corinne G., additional, Hwang, Loris Y., additional, Hynes, Noreen A., additional, James, Peter, additional, Jewell, Elizabeth, additional, Johnson, Susan K., additional, Joshi, Pamela, additional, Joshu, Corinne E., additional, Kamb, Mary L., additional, Karvonen-Gutierrez, Carrie, additional, Kessler, Ronald C., additional, Khandker, Maheruh, additional, Khoury, Samia J., additional, Klein, Autumn M., additional, Koloski, Natasha A., additional, Kuh, Diana, additional, Kulkarni, Jayashri, additional, Kuller, Lewis H., additional, Lacey, James V., additional, LaCroix, Andrea Z., additional, Laden, Francine, additional, Lash, Timothy L., additional, Laughlin-Tommaso, Shannon K., additional, Lee, Cathy C., additional, Lee, Ji Youn, additional, Lee, Stephanie L., additional, LeResche, Linda, additional, Leveille, Suzanne G., additional, Lewis, Jannet F., additional, Lin, Frank R., additional, Tessler Lindau, Stacy, additional, Lindbohm, Marja-Liisa, additional, Liu, Simin, additional, Lloyd-Jones, Donald M., additional, Lortet-Tieulent, Joannie, additional, Lucas, Andrea, additional, Mackey, Rachel H., additional, Mager Stellman, Jeanne, additional, Malarcher, Ann Marie, additional, Manson, JoAnn E., additional, Margesson, Lynette J., additional, Maria Glymour, M., additional, Marrazzo, Jeanne M., additional, Matthews, Karen, additional, Mazzeo, Suzanne E., additional, McCarthy, Ellen P., additional, McCormack, Valerie, additional, McElrath, Thomas F., additional, McMaster, Romy-Leigh, additional, McTigue, Kathleen M., additional, Merikangas, Kathleen Ries, additional, Merz, C. Noel Bairey, additional, Messing, Karen, additional, Miller, Anthony B., additional, Mishell, Daniel R., additional, Missmer, Stacey A., additional, Mobley, Connie, additional, Moscicki, Anna-Barbara, additional, Muffly, Tyler, additional, Muzny, Christina A., additional, Nelson, Amanda E., additional, Nelson, Toben F., additional, O’Dell, Katharine K., additional, Olsen, Catherine M., additional, Olson, Sara H., additional, Osypuk, Theresa L., additional, Palmer, Julie R., additional, Paramsothy, Pangaja, additional, Parke, Ann L., additional, Patrick, Heather, additional, Paulus, Jessica K., additional, Paxton, Lynn, additional, Pearce, Neil, additional, Perti, Tara, additional, Pitzer, Lindsay, additional, Platz, Elizabeth A., additional, Potischman, Nancy, additional, Punnett, Laura, additional, Ramsey-Goldman, Rosalind, additional, Ranji, Usha, additional, Rastogi, Radhai M., additional, Reckelhoff, Jane F., additional, Resnick, Barbara, additional, Rexrode, Kathryn M., additional, Rigterink, Ellen S., additional, Rillamas-Sun, Eileen, additional, Robinson, Cara A., additional, Robinson, Jennifer G., additional, Robson, Mark E., additional, Rompalo, Anne M., additional, Saftlas, Audrey F., additional, Salganicoff, Alina, additional, Sallmén, Markku, additional, Sanjosé, Silvia de, additional, Sarto, Gloria E., additional, Sass, Samantha, additional, Savage, Sharon A., additional, Schildkraut, Joellen, additional, Schmaling, Karen, additional, Schmitz, Anja, additional, Scholl, Theresa O., additional, Schwebke, Jane R., additional, Scott, Stacey B., additional, Seedat, Soraya, additional, Seeman, Mary V., additional, Seow, Adeline, additional, Shah, Rashmee U., additional, Collins Sharp, Beth A., additional, Shin, Hai-Rim, additional, Shoupe, Donna, additional, Silverman, Debra T., additional, Snow, Rachel C., additional, Sophia, Eglacy C., additional, Sowers, MaryFran R., additional, Spaderna, Heike, additional, Stahre, Mandy, additional, Stewart, Elizabeth G., additional, Stuenkel, Cynthia A., additional, Stussman, Barbara, additional, Suliman, Sharain, additional, Talley, Nicholas J., additional, Taskinen, Helena, additional, Tatpati, Laura L., additional, Thomeer, Mieke Beth, additional, Titus, Linda J., additional, Tjaden, Bruce L., additional, Trabert, Britton, additional, Trace, Sara E., additional, Traverse, William, additional, Troisi, Rebecca, additional, Troped, Philip J., additional, Umberson, Debra, additional, Upson, Kristen, additional, Wagenen, Aimee Van, additional, Wald, Anna, additional, Wang, James K.C., additional, Ward, Mary H., additional, Wei, Shu-Qin, additional, Weidner, Gerdi, additional, Wentzensen, Nicolas, additional, Whiteside, James L., additional, Williams, Kristi, additional, Windham, Gayle C., additional, Wiringa, Ann E., additional, Wise, Lauren A., additional, Wofford, Marion, additional, Wu, Anna H., additional, Yaffe, Kristine, additional, Yang, Frances M., additional, Yunus, Muhammad B., additional, Zahm, Shelia Hoar, additional, Zera, Chloe A., additional, and Zilberman, Monica L., additional
- Published
- 2013
- Full Text
- View/download PDF
40. Sexual dimorphism in the renin-angiotensin system in aging spontaneously hypertensive rats
- Author
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Yanes, Licy L., Romero, Damian G., Iles, Joshua W., Iliescu, Radu, Gomez-Sanchez, Celso, and Reckelhoff, Jane F.
- Subjects
Dimorphism (Biology) -- Research ,Angiotensin -- Receptors ,Angiotensin -- Research ,Biological sciences - Abstract
In young adult spontaneously hypertensive rats (SHR), mean arterial pressure (MAP) is higher in males than in females and inhibition of the renin-angiotensin system (RAS) eliminates this sex difference. After cessation of estrous cycling in female SHR, MAP is similar to that in male SHR. The purpose of this study was to determine the role of the RAS in maintenance of hypertension in aging male and female SHR. At 16 mo of age, MAP was similar in male and female SHR (183 [+ or -] 5 vs. 193 [+ or -] 8 mmHg), and chronic losartan (40 mg x [kg.sup.-1] x [day.sup.-1] po for 3 wk) reduced MAP by 52% (to 90 [+ or -] 8 mmHg, P < 0.05 vs. control) in males and 37% (to 123 [+ or -] 11 mmHg, P < 0.05 vs. control) in females (P < 0.05, females vs. males). The effect of losartan on angiotensin type 1 ([AT.sub.1]) receptor blockade was similar: MAP responses to acute doses of ANG II (62.5-250 ng/kg) were blocked to a similar extent in losartan-treated males and females. [F.sub.2]-isoprostane excretion was reduced with losartan more in males than in females. There were no sex differences in plasma renin activity, plasma angiotensinogen or ANG II, or renal expression of [AT.sub.1] receptors, angiotensin-converting enzyme, or renin. However, renal angiotensinogen mRNA and protein expression was higher in old males than females, whereas renal ANG II was higher in old females than males. The data show that, in aging SHR, when blood pressures are similar, there remains a sexual dimorphism in the response to [AT.sub.1] receptor antagonism, and the differences may involve sex differences in mechanisms responsible for oxidative stress with aging. sex differences; angiotensin type 1 receptor; angiotensinogen; angiotensin II; oxidative stress doi:10.1152/ajpregu.00510.2005
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- 2006
41. Role of the renal nerves in blood pressure in male and female SHR
- Author
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Iliescu, Radu, Yanes, Licy L., Bell, William, Dwyer, Terry, Baltatu, Ovidiu C., and Reckelhoff, Jane F.
- Subjects
Rats -- Research ,Rattus -- Research ,Blood pressure -- Research ,Dimorphism (Biology) -- Research ,Biological sciences - Abstract
Female spontaneously hypertensive rats (SHR) have lower blood pressures than males. The renin-angiotensin system plays an important role in the sexual dimorphism of blood pressure in SHR. The sympathetic nervous system can stimulate renin release, and, therefore, the present study was performed to determine whether the renal sympathetic nerves play a role in the sexual dimorphism of blood pressure in SHR. Male and female SHR underwent bilateral kidney denervation or sham surgery, and, 2 wk later, mean arterial pressure (MAP) and pulse interval were recorded, and baroreflex sensitivity (BRS) was measured by the sequence technique. Left ventricle index (LVI) was also calculated. MAP was higher in sham-operated males than females (182 [+ or -] 5 vs. 169 [+ or -] 4 mmHg; P < 0.01), but, despite the higher MAP in males, LVI was significantly greater in female rats. BRS was not different between sham-operated male and female SHR. Following bilateral renal denervation, MAP was decreased by a similar percentage (8-10%) in males (169 [+ pr -] 2 mmHg) and females (152 [+ or -] 3 mmHg), whereas LVI was reduced only in female SHR. BRS was not altered by renal denervation in either sex. These data indicate that renal nerves play a role in the control of blood pressure in SHR independent of sex, but do not play a role in mediating the sex differences in blood pressure. baroreflex sensitivity; mean arterial pressure; sexual dimorphism; renal denervation
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- 2006
42. Testosterone supplementation in aging men and women: possible impact on cardiovascular-renal disease
- Author
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Reckelhoff, Jane F., Yanes, Licy L., Iliescu, Radu, Fortepiani, Lourdes A., and Granger, Joey P.
- Subjects
Antiandrogens -- Usage ,Osteoporosis -- Care and treatment ,Postmenopausal women -- Health aspects ,Biological sciences - Abstract
Treatment of aging men and women with testosterone supplements is increasing. The supplements are given to postmenopausal women mainly to improve their libido and to aging men to improve muscle mass and bone strength, to improve libido and quality of life, to prevent and treat osteoporosis, and, with the phosphodiesterase-5 inhibitors, such as sildenafil, to treat erectile dysfunction. The increased use of testosterone supplements in aging individuals has occurred despite the fact that there have been no rigorous clinical trials examining the effects of chronic testosterone on the cardiovascular-renal disease risk. Studies in humans and animals have suggested that androgens can increase blood pressure and compromise renal function. Androgens have been shown to increase tubular sodium and water reabsorption and activate various vasoconstrictor systems in the kidney, such as the renin-angiotensin system and endothelin. There is also evidence that androgens may increase oxidative stress. Furthermore, the kidney contains the enzymes necessary to produce androgens de novo. This review presents an overview of the data from human and animal studies in which the role of androgens in promoting renal and cardiovascular diseases has been investigated. androgen receptor; oxidative stress; angiotensin II; endothelin; cytokines
- Published
- 2005
43. Increasing oxidative stress with molsidomine increases blood pressure in genetically hypertensive rats but not normotensive controls
- Author
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Fortepiani, Lourdes A. and Reckelhoff, Jane F.
- Subjects
Dimorphism (Biology) -- Research ,Hypertension -- Research ,Oxidative stress -- Research ,Biological sciences - Abstract
Spontaneously hypertensive rats (SHR) have a higher level of oxidative stress and exhibit a greater depressor response to a superoxide scavenger, tempol, than normotensive Wistar-Kyoto rats (WKY). This study determined whether an increase in oxidative stress with a superoxide/NO donor, molsidomine, would amplify the blood pressure in SHR. Male SHR and WKY were given molsidomine (30 mg x [kg.sup.-1] x [day.sup.-1]) or vehicle (0.01% ethanol) for 1 wk, and blood pressure, renal hemodynamics, nitrate and nitrite excretion (NOx), renal superoxide production, and expression of renal antioxidant enzymes, Mn- and Cu,Zn-SOD, catalase, and glutathione peroxidase (GPx), were measured. Renal superoxide and NOx were higher in control SHR than in WKY. Molsidomine increased superoxide by ~35% and NOx by 250% in both SHR and WKY. Mean arterial blood pressure (MAP) was also higher in control SHR than WKY. Molsidomine increased MAP by 14% and caused renal vasoconstriction in SHR but reduced MAP by 16%, with no effect on renal hemodynamics, in WKY. Renal expression of Mn- and Cu,Zn-SOD was not different between SHR and WKY, but expression of catalase and GPx were ~30% lower in kidney of SHR than WKY. The levels of Mn- and Cu,Zn-SOD were not increased with molsidomine in either WKY or SHR. Renal catalase and GPx expression was increased by 300-400% with molsidomine in WKY, but there was no effect in SHR. Increasing oxidative stress elevated blood pressure further in SHR but not WKY. WKY are likely protected because of higher bioavailable levels of NO and the ability to upregulate catalase and GPx. sexual dimorphism; glomerular filtration rate; catalase; glutathione peroxidase
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- 2005
44. Systemic arterial pressure response to two weeks of Tempol therapy in SHR: involvement of NO, the RAS, and oxidative stress
- Author
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Yanes, Licy, Romero, Damian, Iliescu, Radu, Cucchiarelli, Valeria E., Fortepiani, Lourdes A., Santacruz, Francisco, Bell, William, Zhang, Huimin, and Reckelhoff, Jane F.
- Subjects
Renin-angiotensin system -- Research ,Renin-angiotensin system -- Physiological aspects ,Nitric oxide -- Research ,Nitric oxide -- Physiological aspects ,Hypertension -- Research ,Hypertension -- Physiological aspects ,Hypertension -- Drug therapy ,Biological sciences - Abstract
The roles of nitric oxide (NO) and plasma renin activity (PRA) in the depressor response to chronic administration of Tempol in spontaneously hypertensive rats (SHR) are not clear. The present study was done to determine the effect of 2 wk of Tempol treatment on blood pressure [mean arterial pressure (MAP)], oxidative stress, and PRA in the presence or absence of chronic NO synthase inhibition. SHR were divided into four groups: control, Tempol (1 mmol/1) alone, nitro-L-arginine methyl ester (L-NAME, 4.5 mg x [kg.sup.-1] x [day.sup.-1]) alone, and Tempol + L-NAME for 2 wk. With Tempol, MAP decreased by 22%: 191 [+ or -] 3 and 162 [+ or -] 21 mmHg for control and Tempol, respectively (P < 0.05). L-NAME increased MAP by 16% (222 [+ or -] 2 mmHg, P < 0.01), and L-NAME + Tempol abolished the depressor response to Tempol (215 [+ or -] 3 mmHg, P < 0.01). PRA was not affected by Tempol but was increased slightly with L-NAME alone and 4.4-fold with L-NAME + Tempol. Urinary nitrate/nitrite increased with Tempol and decreased with L-NAME and L-NAME + Tempol. Tempol significantly reduced oxidative stress in the presence and absence of L-NAME. In conclusion, in SHR, Tempol administration for 2 wk reduces oxidative stress in the presence or absence of NO, but in the absence of NO, Tempol is unable to reduce MAP. Therefore, NO, but not changes in PRA, plays a major role in the blood pressure-lowering effects of Tempol. These data suggest that, in hypertensive individuals with endothelial damage and chronic NO deficiency, antioxidants may be able to reduce oxidative stress but not blood pressure. nitric oxide; superoxide; antioxidant; renin-angiotensin system
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- 2005
45. Role of endothelin in mediating postmenopausal hypertension in a rat model
- Author
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Yanes, Licy L., Romero, Damian G., Cucchiarelli, Valeria E., Fortepiani, Lourdes A., Gomez-Sanchez, Celso E., Santacruz, Francisco, and Reckelhoff, Jane F.
- Subjects
Rats -- Research ,Rattus -- Research ,Postmenopausal women -- Health aspects ,Kidneys -- Physiological aspects ,Death -- Risk factors ,Women -- Health aspects ,Cardiovascular diseases ,Biological sciences - Abstract
Cardiovascular disease is the leading cause of death in women after menopause. Hypertension, a major cardiovascular risk factor, becomes more prevalent after menopause. The mechanisms responsible for the increase in blood pressure (BP) in postmenopausal women are unknown. We have recently characterized the aged, postestrous-cycling (PMR) spontaneously hypertensive rats (SHR) as a model of postmenopausal hypertension. The purpose of the present study was to determine whether endothelin plays a role in the increased BP in PMR. Premenopausal female SHR, aged 4-5 mo (YF), and PMR, aged 16 too, were studied. Expression of preproendothelin-1 mRNA was not different in either renal cortex or medulla between PMR and YF (n = 7-8/group). In contrast, ET-1 peptide expression was significantly higher in renal cortex of PMR than in renal cortex of YF, but there was no difference in medullary ET-1. Expression of endothelin E[T.sub.A] receptor (E[TA.sub.]R) mRNA was lower in renal cortex and medulla of PMR than of YF. Additional groups of rats (n = 6-7/group) were treated for 3 wk with the ETAR antagonist ABT-627 (5 mg x [kg.sup.-1] x [day.sup.-1]). BP was significantly higher in PMR than in YF. ETAR antagonist reduced BP in PMR by 20% to the level found in control YF. E[T.sub.A]R antagonist had no effect on BP in YF. These data support the hypothesis that the increase in BP in PMR is mediated in part by endothelin and the E[T.sub.A]R. E[T.sub.A] receptor; ETB receptor; kidney
- Published
- 2005
46. Role of oxidative stress in age-related reduction of NO-cGMP-mediated vascular relaxation in SHR
- Author
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Payne, Jason A., Reckelhoff, Jane F., and Khalil, Raouf A.
- Subjects
Smooth muscle -- Physiological aspects ,Nitric oxide -- Physiological aspects ,Cookery for hypertensives -- Physiological aspects ,Hypertension -- Physiological aspects ,Biological sciences - Abstract
The incidence of hypertension increases during the late stages of aging; however, the vascular mechanisms involved are unclear. We investigated whether the late stages of aging are associated with impaired nitric oxide (NO)-mediated vascular relaxation and enhanced vascular contraction and whether oxidative stress plays a role in the age-related vascular changes. Aging (16 mo) male spontaneously hypertensive rats (SHR) nontreated or treated for 8 mo with the antioxidant tempol (1 mM in drinking water) or vitamin E (E; 5,000 IU/kg chow) and vitamin C (C; 100 mg*[kg.sup.-1]*[day.sup.-1] in drinking water) and adult (12 wk) male SHR were used. After the arterial pressure was measured, aortic strips were isolated from the rats for measurement of isometric contraction. The arterial pressure and phenylephrine (Phe)-induced vascular contraction were enhanced, and the ACh-induced vascular relaxation and nitrite/nitrate production were reduced in aging compared with adult rats. In aging rats, the arterial pressure was nontreated (188 [+ or -] 4), tempol-treated (161 [+ or -] 6), and E + C-treated (187 [+ or -] 1 mmHg). Phe ([10.sup.-5] M) caused an increase in active stress in nontreated aging rats (14.3 [+ or -] 1.0) that was significantly (P < 0.05) reduced in tempol-treated (9.0 [+ or -] 0.7) and E + C-treated rats (9.8 [+ or -] 0.6 x [10.sup.4] N/[m.sup.2]). ACh produced a small relaxation of Phe contraction in non-treated aging rats that was enhanced (P < 0.05) in tempoland E + C-treated rats. L-NAME ([10.sup.-4] M), inhibitor of NO synthase, or ODQ ([10.sup.-5] M), inhibitor of cGMP production in smooth muscle, inhibited ACh relaxation and enhanced Phe contraction in tempol- and E + C-treated but not the nontreated aging rats. ACh-induced vascular nitrite/nitrate production was not different in nontreated, tempol-and E + C-treated aging rats. Relaxation of Phe contraction with sodium nitroprusside, an exogenous NO donor, was smaller in aging than adult rats but was not different between nontreated, tempol- and E + C-treated aging rats. Thus, during the late stages of aging in SHR rats, an age-related inhibition of a vascular relaxation pathway involving not only NO production by endothelial cells but also the bioavailability of NO and the smooth muscle response to NO is partially reversed during chronic treatment with the antioxidants tempol and vitamins E and C. The data suggest a role for oxidative stress in the reduction of vascular relaxation and thereby the promotion of vascular contraction and hypertension during the late stages of aging. arterial pressure; endothelium; nitric oxide; vascular smooth muscle; contraction; spontaneously hypertensive rats
- Published
- 2003
47. Role of oxidative stress in angiotensin-induced hypertension
- Author
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Reckelhoff, Jane F. and Romero, J. Carlos
- Subjects
Physiology -- Research ,Oxidation-reduction reaction -- Physiological aspects ,Hypertension -- Physiological aspects ,Endothelin -- Physiological aspects ,Cookery for hypertensives ,Biological sciences - Abstract
Infusion of ANG II at a rate not sufficient to evoke an immediate vasoconstrictor response, produces a slow increase in blood pressure. Circulating levels of ANG II may be within ranges found in normotensive individuals, although inappropriately high with respect to sodium intake. When ANG II levels are dissociated from sodium levels, oxidative stress (OXST) occurs, which can increase blood pressure by several mechanisms. These include inadequate production or reduction of bioavailability of nitric oxide, alterations in metabolism of arachidonic acid, resulting in an increase in vasoconstrictors and decrease in vasodilators, and upregulation of endothelin. This cascade of events appears to be linked, because ANG II hypertension can be blocked by inhibition of any factor located distally, blockade of ANG II, OXST, or endothelin. Such characteristics are shared by other models of hypertension, such as essential hypertension, hypertension induced by reduction in renal mass, and renovascular hypertension. Thus these findings are clinically important because they reveal 1) uncoupling between ANG II and sodium, which can trigger pathological conditions; 2) the various OXST mechanisms that may be involved in hypertension; and 3) therapeutic interventions for hypertension developed with the knowledge of the cascade involving OXST. isoprostanes; endothelin; spontaneous hypertension; renovascular hypertension; sodium balance
- Published
- 2003
48. Testosterone Supplementation in Male Obese Zucker Rats Reduces Body Weight and Improves Insulin Sensitivity But Increases Blood Pressure
- Author
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Davis, Deborah D., Lopez Ruiz, Arnaldo, Yanes, Licy L., Iliescu, Radu, Yuan, Kuichang, Moulana, Mohadetheh, Racusen, Lorraine C., and Reckelhoff, Jane F.
- Published
- 2012
- Full Text
- View/download PDF
49. Chapter 1 - Androgens and Cardiovascular Diseases in Women
- Author
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Yanes Cardozo, Licy L., Torres Fernandez, Edgar D., Romero, Damian G., and Reckelhoff, Jane F.
- Published
- 2019
- Full Text
- View/download PDF
50. Abstract P209: Androgen Receptor Antagonist, Bicalutamide, And Androgen Receptor Degradation Enhancer, Asc-j9, Decrease Blood Pressure Similarly In Male Spontaneously-hypertensive Rats.
- Author
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Shawky, Noha M, primary and Reckelhoff, Jane F, additional
- Published
- 2020
- Full Text
- View/download PDF
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