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51. List of Contributors

Author

Abdala, Ana P.L., primary, Adams, David H., additional, Alvarenga, Marlies, additional, Arnold, Amy C., additional, Axelrod, Felicia B., additional, Barbic, Franca, additional, Barnes, Peter J., additional, Bauer, Deborah, additional, Bell, Christopher, additional, Benarroch, Eduardo E., additional, Berry-Kravis, Elizabeth M., additional, Bernardi, Luciano, additional, Biaggioni, Italo, additional, Birder, Lori, additional, Brooks, Virginia L., additional, Heller Brown, Joan, additional, Burnstock, Geoffrey, additional, Camilleri, Michael, additional, Campbell, J.Preston, additional, Carey, Robert M., additional, Caron, Marc G., additional, Carter, Calvin, additional, Cassaglia, Priscila A., additional, Castillo, Javier G., additional, Chapleau, Mark W., additional, Charkoudian, Nisha, additional, David Charles, P., additional, Chelimsky, Gisela, additional, Chelimsky, Thomas, additional, Cheng, Pei-Wen, additional, Clément, Gilles, additional, Cortelli, Pietro, additional, Cowley, Allen W., additional, Crews, Leslie, additional, Davis, Stephen N., additional, Davis, Thomas L., additional, de Groat, William C., additional, DeMarco, Vincent G., additional, Diedrich, André, additional, DiPette, Donald J., additional, Diz, Debra I., additional, Drake, Marcus J., additional, Drew, Rachel C., additional, Dütsch, Matthias, additional, Eisenhofer, Graeme, additional, Elefteriou, Florent, additional, Elijovich, Fernando, additional, English, Brett A., additional, Esler, Murray, additional, Fang, John Y., additional, Fealey, Robert D., additional, Fernandez, Stanley, additional, Fink, Gregory D., additional, Floras, John S., additional, Freeman, Roy, additional, Fu, Qi, additional, Fu, Liang-Wu, additional, Furlan, Raffaello, additional, Gamboa, Alfredo, additional, Garland, Emily M., additional, Gibbons, Christopher H., additional, Gilbey, Michael P., additional, Gilden, Janice L., additional, Gilman, Sid, additional, Goldstein, David S., additional, Golombek, Diego A., additional, Graham, Robert M., additional, Grassi, Guido, additional, Grier, Mark D., additional, Groothuis, Jan T., additional, Grubb, Blair P., additional, Hahn, Maureen K., additional, Halcox, Julian P.J., additional, Hamill, Robert W., additional, Hande, Kenneth R., additional, Harati, Yadollah, additional, Harrison, David G., additional, Hart, Emma C., additional, Hastings, Jacqui, additional, Henderson, Luke A., additional, Hilz, Max J., additional, Hoeldtke, Robert, additional, Ho, Shung Tai, additional, Hunter, Peter, additional, Hyland, Keith, additional, Hyland, Lauren, additional, Izadyar, Shahram, additional, Izzo, Joseph L., additional, Jackson, Edwin K., additional, Jacob, Giris, additional, Jänig, Wilfrid, additional, Johnson, Megan S., additional, Jones, Carrie K., additional, Jones, James F.X., additional, Joos, Karen M., additional, Jordan, Jens, additional, Joyner, Michael J., additional, Kaler, Stephen G., additional, Kasparov, Sergey, additional, Kaufmann, Horacio, additional, Kaye, David, additional, Khurana, Ramesh K., additional, Kim, Chun-Hyung, additional, Kim, Kwang-Soo, additional, Kobayashi, Kazuto, additional, Kuntz, Nancy L., additional, Konecny, Tomas, additional, Kontak, Andrew, additional, Laffer, Cheryl L., additional, Lagrange, Andre H., additional, Laiken, Nora, additional, Lambert, Gavin, additional, Lenders, Jacques W.M., additional, Levine, Benjamin D., additional, Lipsitz, Lewis A., additional, Lombard, Julian H., additional, Longhurst, John C., additional, Low, David A., additional, Low, Phillip A., additional, Lu, Chih Cherng, additional, Luther, James M., additional, Macefield, Vaughan G., additional, McCully, Belinda H., additional, McLeod, James G., additional, Manger, William M., additional, Mano, Tadaaki, additional, Marvar, Paul J., additional, Masliah, Eliezer, additional, Mathias, Christopher J., additional, Melson, Mark R., additional, Milam, Douglas F., additional, Mohl, Marion C., additional, Molkov, Yaroslav I., additional, Morris, Margaret, additional, Morrison, Shaun F., additional, Nagatsu, Toshiharu, additional, Nichols, Charles D., additional, Norcliffe-Kaufmann, Lucy, additional, Novak, Vera, additional, Okamoto, Luis E., additional, Osborn, John W., additional, Parsons, Brian A., additional, Paton, Julian F.R., additional, Patwari, Pallavi P., additional, Phan, Cecile L., additional, Phibbs, Fenna T., additional, Prabhakar, Nanduri R., additional, Peltier, Amanda C., additional, Peterson, Sean M., additional, Pickering, Anthony E, additional, Pratt, J.Howard, additional, Rahmouni, Kamal, additional, Raj, Satish R., additional, Rand, Casey M., additional, Reichmann, Heinz, additional, Richards, Jeff, additional, Roberts, L.Jackson, additional, Robertson, David W., additional, Robertson, Rose Marie, additional, Robinson, Michael, additional, Rybak, Ilya A., additional, Sanders-Bush, Elaine, additional, Sandroni, Paola, additional, Sato, Kyoko, additional, Sato, Takayuki, additional, Schatz, Irwin J., additional, Schiffrin, Ernesto L., additional, Schondorf, Ronald, additional, Schwarz, Rosemary, additional, Seravalle, Gino, additional, Shapiro, Robert E., additional, Shibao, Cyndya, additional, Somers, Virend, additional, Stampfer, Michaela, additional, Stein, C.Michael, additional, Stemberger, Sylvia, additional, Stewart, Julian, additional, Sinoway, Lawrence I., additional, Sowers, James R., additional, Srikakarlapudi, Sirisha, additional, Sunagawa, Kenji, additional, Supowit, Scott C., additional, Taylor, Palmer, additional, Thompson, Jane, additional, Thijs, Roland D., additional, Touyz, Rhian M, additional, Tranel, Daniel, additional, Trikudanathan, Subbulaxmi, additional, Tseng, Ching-Jiunn, additional, Tung, Che-Se, additional, Ubhi, Kiren, additional, Urs, Nikhil, additional, Verbalis, Joseph G., additional, Vernino, Steven, additional, Victor, Ronald G., additional, Vizzard, Margaret A., additional, Vongpatanasin, Wanpen, additional, Wallin, B.Gunnar, additional, Wang, Tobias, additional, Wang, Qin, additional, Webster, Andrew A., additional, Weese-Mayer, Debra E., additional, Wenning, Gregor K., additional, Whaley-Connell, Adam, additional, Wieling, Wouter, additional, Williams, Gordon H., additional, Wood, Scott, additional, Ziegler, Michael G., additional, and Zoccal, Daniel B., additional

Published
2012
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53. Angiotensin receptors contribute to blood pressure homeostasis in salt-depleted SHR

Author

Nakamura, Shigefumi, Averill, David B., Chappell, Mark C., Diz, Debra I., Brosnihan, K. Bridget, and Ferrario, Carlos M.

Subjects
Angiotensin -- Physiological aspects, Rats -- Physiological aspects, Rattus, Heart beat -- Physiological aspects, Heart -- Physiological aspects, Biological sciences
Abstract

This study evaluated the contribution of angiotensin peptides acting at various receptor subtypes to the arterial pressure and heart rate of adult 9-wk-old male conscious salt-depleted spontaneously hypertensive rats (SHR). Plasma ANG II and ANG I in salt-depleted SHR were elevated sevenfold compared with peptide levels measured in sodium-replete SHR, whereas plasma ANG-(1-7) was twofold greater in salt-depleted SHR compared with salt-replete SHR. Losartan (32.5 [micro]mol/kg), PD-123319 (0.12 [micro]mol.[kg.sup.-1] [min.sup.-1]), [D-[Ala.sup.7]]ANG-(1-7) (10 and 100 [micro]mol/min), and a polyclonal ANG II antibody (0.08 mg/min) were infused intravenously alone or in combination. Combined blockade of A[T.sub.2] and A[T.sub.(1-7)] receptors significantly increased the blood pressure of losartan-treated SHR (+ 15 [+ or -] 1 mmHg; P < 0.01); this change did not differ from the blood pressure elevation produced by the sole blockade of A[T.sub.(1-7)] receptors (15 [+ or -] 4 mmHg). On the other hand, sole blockade of A[T.sub.2] receptors in losartan-treated SHR increased mean arterial pressure by 8 [+ or -] 1 mmHg (P < 0.05 vs. 5% dextrose in water as vehicle), and this increase was less than the pressor response produced by blockade of A[T.sub.(1-7)] receptors alone or combined blockade of A[T.sub.(1-7)] and A[T.sub.2] receptors. The ANG II antibody increased blood pressure to the greatest extent in salt-depleted SHR pretreated with only losartan (+ 11 [+ or -] 2 mmHg) and to the least extent in salt-depleted SHR previously treated with the combination of losartan, PD-123319, and [D-[Ala.sup.7]]ANG-(1-7) (+7 [+ or -] 1 mmHg; P < 0.01). Losartan significantly increased heart rate, whereas other combinations of receptor antagonists or the ANG II antibody did not alter heart rate. Our results demonstrate that ANG II and ANG-(1-7) act through non-A[T.sub.1] receptors to oppose the vasoconstrictor actions of ANG II in salt-depleted SHR. Combined blockade of A[T.sub.2] and A[T.sub.(1-7)] receptors and ANG II neutralization by the ANG II antibody reversed as much as 67% of the blood pressure-lowering effect of losartan. angiotensin II; angiotensin-(1-7); angiotensin receptor antagonists; hypertension; losartan; PD-123319; salt depletion; spontaneously hypertensive rats

Published
2003

54. Children with chronic nausea and orthostatic intolerance have unique brain network organization: A case‐control trial.

Author

Fortunato, John E., Laurienti, Paul J., Wagoner, Ashley L., Shaltout, Hossam A., Diz, Debra I., Silfer, Jessy L., and Burdette, Jonathan H.

Subjects
ORTHOSTATIC intolerance, LARGE-scale brain networks, FRONTOPARIETAL network, DEFAULT mode network, SALIENCE network, FUNCTIONAL connectivity
Abstract

Background: Determine whether subjects with chronic nausea and orthostatic intolerance share common alterations in key brain networks associated with central autonomic control: default mode, salience, and central executive networks, and the insula, a key component of the salience network. Methods: Ten subjects (ages 12–18 years; 8 females, 2 males) with nausea predominant dyspepsia, orthostatic intolerance, and abnormal head‐upright tilt test were consecutively recruited from pediatric gastroenterology clinic. These subjects were compared with healthy controls (n = 8) without GI symptoms or orthostatic intolerance. Resting‐state fMRI and brain network modularity analyses were performed. Differences in the default mode, salience, and central executive networks, and insular connectivity were measured. Key Results: The community structure of the default mode network and salience network was significantly different between tilt‐abnormal children and controls (p = 0.034 and 0.012, respectively), whereas, no group difference was observed in the central executive network (p = 0.48). The default mode network was more consistently "intact," and the consistency of the community structure in the salience network was reduced in tilt‐abnormal children, especially in the insula. Conclusions and Inferences: Children with chronic nausea and orthostatic intolerance have altered connectivity in the default mode network and salience network/insula, which supports over‐monitoring of their body and altered processing of bodily states resulting in interoceptive hyper self‐awareness. The connectivity of the salience network would not support optimal regulation of appropriate attention to internal and external stimuli, and the hyper‐connected default mode network may result in a persistent self‐referential state with feelings of emotion, pain, and anxiety. [ABSTRACT FROM AUTHOR]

Published
2022
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61. Contributors

Author

Asmar, Roland, primary, Basile, Jan N., additional, Beevers, D.G., additional, Beilin, Lawrence J., additional, Bilo, Grzegorz, additional, Black, Henry R., additional, Boerrigter, Guido, additional, Bone, Lee R., additional, Brunner, Hans, additional, Burnett, John C., additional, Calhoun, David A., additional, Campese, Vito M., additional, Carey, Robert M., additional, Caro, J. Jaime, additional, Carretero, Oscar A., additional, Chappell, Mark C., additional, Chrysant, George S., additional, Cutler, Jeffrey A., additional, Dahlöf, Björn, additional, da Silva, Alexandre A., additional, de Faire, Ulf, additional, Delgado, Maria Carolina, additional, Devereux, Richard B., additional, Diamond, Joseph A., additional, DiPette, Donald J., additional, Diz, Debra I., additional, Edelman, Jonathan M., additional, Elliott, William J., additional, Ekman, Steffan, additional, Falkner, Bonita, additional, Fan, William L., additional, Fenichel, Robert R., additional, Ferrario, Carlos M., additional, Franklin, Stanley S., additional, Freis, Edward D., additional, Frishman, William H., additional, Frohlich, Edward D., additional, Funder, John W., additional, Fyhrquist, Frej, additional, Gamba, Gerardo, additional, Gami, Apoor S., additional, Gavras, Haralambos, additional, Gavras, Irene, additional, Gehr, Todd W.B., additional, Gleim, Gilbert W., additional, Hall, John E., additional, Hanes, Donna S., additional, Harrap, tephen B., additional, Harris, Katherine E., additional, Haus, Erhard, additional, Hermida, Ramon C., additional, Hill, Martha N., additional, Ibsen, Hans, additional, Intengan, Hope, additional, Izzo, Joseph L., additional, Jennings, Garry L.R., additional, Johnson, Ernest F., additional, Johnston, Colin I., additional, Jones, Daniel W., additional, Julius, Stevo, additional, Kannel, William B., additional, Katki, Khurshed A., additional, Kjeldsen, Sverre E., additional, Kleyman, Thomas R., additional, Knepper, Mark A., additional, Kokkoris, Panagiotis, additional, Kostis, John B., additional, Krakoff, Lawrence R., additional, Kristianson, Krister J., additional, Kuo, Jay J., additional, Lakkis, Jay, additional, Laragh, John H., additional, Levine, David M., additional, Light, Kathleen C., additional, Lindholm, Lars H., additional, Liu, Jiankang, additional, Lüscher, Thomas F., additional, Mancia, Giuseppe, additional, Mansoor, George A., additional, McCarron, David A., additional, McGuire, Heather L., additional, McInnes, Gordon T., additional, McMahon, Ellen G., additional, Meyer, Renee P., additional, Miller, Nancy Houston, additional, Nadim, Mitra K., additional, Nesbitt, Shawna D., additional, Neutel, Joel M., additional, Nieminen, Markku S., additional, Nussberger, Jürg, additional, Omvik, Per, additional, Oparil, Suzanne, additional, Opie, Lionel H., additional, Osterberg, Lars, additional, Parati, Gianfranco, additional, Payne, Krista A., additional, Pedersen, Ole Lederballe, additional, Phillips, Robert A., additional, Pi-Sunyer, Xavier, additional, Plat, Francis, additional, Pool, James L., additional, Portaluppi, Francesco, additional, Prisant, L. Michael, additional, Puddey, Ian B., additional, Raj, Satish R., additional, Reaven, Gerald M., additional, Reeves, Scott T., additional, Reinberg, Alain, additional, Reiser, Ira W., additional, Reudelhuber, Timothy L., additional, Reusser, Molly E., additional, Reves, J.G., additional, Rhaleb, Nour-Eddine, additional, Robertson, David, additional, Roccella, Edward J., additional, Rudd, Peter, additional, Ruddy, Michael C., additional, Ruilope, Luis Miguel, additional, Schiffrin, Ernesto L., additional, Schirger, John A., additional, Schork, M. Anthony, additional, Shepherd, Alexander M.M., additional, Sica, Domenic A., additional, Siragy, Helmy M., additional, Smith, Beverly A., additional, Smolensky, Michael H., additional, Snapinn, Steven, additional, Somers, Virend K., additional, Spieker, Lukas E., additional, Spitalewitz, Samuel, additional, Stolt, Pelle, additional, Supowit, Scott C., additional, Svetkey, Laura P., additional, Taler, Sandra J., additional, Tallam, Lakshmi S., additional, Tallant, E. Ann, additional, Tikellis, Chris, additional, Turnbull, Fiona, additional, Vidt, Donald G., additional, Watson, Ralph E., additional, Weber, Michael A., additional, Wedel, Hans, additional, Weder, Alan B., additional, Weinberger, Myron H., additional, Weir, Matthew R., additional, White, William B., additional, Wofford, Marion R., additional, Wong, Nathan D., additional, Wright, Jackson T., additional, Yang, Xiao-Ping, additional, Young, William F., additional, Zanchetti, Alberto, additional, and Zhao, Huawei, additional

Published
2005
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62. Angiotensin-(1-7)

Author

Diz, Debra I., primary, Chappell, Mark C., additional, Tallant, E. Ann, additional, and Ferrario, Carlos M., additional

Published
2005
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66. Acute depressor actions of angiotensin II in the nucleus of the solitary tract are mediated by substance P

Author

Diz, Debra I., Fantz, Deborah L., Benter, Ibrahim F., and Bosch, Susan M.

Subjects
Substance P -- Antagonists, Angiotensin -- Physiological aspects, Rats -- Physiological aspects, Biological sciences
Abstract

Researchers have investigated whether a specific substance P antagonist can block the actions of angiotensin II (ANG II) exogenously administered into the nucleus of the solitary tract (NTS) of halothane-anesthetized male Sprague-Dawley rats. It was found that the substance P antagonist blocks the acute depressor and bradycardic responses of ANG II almost entirely. This indicates that postsynaptic cells may be a key source of the substance P mediating the acute cardiovascular responses to ANG II.

Published
1997

67. Antihypertensive actions of angiotensin-(1-7) in spontaneously hypertensive rats

Author

Benter, Ibrahim F., Ferrario, Carlos M., Morris, Mariana, and Diz, Debra I.

Subjects
Angiotensin -- Physiological aspects, Hypertension -- Physiological aspects, Biological sciences
Abstract

Angiotensin 1-7 (ANG I-7) is an active depressor heptapeptide in intact animals and may have an important role in the vasodepressor system, inhibiting hemodynamic actions of angiotensin II (ANG II). Experiments on hypertensive rats were conducted to examine the effects of the ANG 1-7 on the maintenance of elevated blood pressures. After infusion with ANG 1-7 for two weeks, researchers observed a reduction in vasopressin, and a lowering then rise in arterial blood pressure.

Published
1995

77. Antenatal corticosteroids and the renin-angiotensin-aldosterone system in adolescents born preterm

Author

O'Shea, T. Michael, Rose, James C., Russell, Gregory B., Chappell, Mark C., Nixon, Patricia A., Shaltout, Hossam A., Diz, Debra I., South, Andrew M., Washburn, Lisa K., and Snively, Beverly M.

Subjects
hemic and lymphatic diseases, reproductive and urinary physiology, female genital diseases and pregnancy complications
Abstract

Antenatal corticosteroid (ANCS) treatment hastens fetal lung maturity and improves survival of premature infants, but the long-term effects of ANCS are not well-described. Animal models suggest ANCS increases the risk of cardiovascular disease through programmed changes in the renin-angiotensin (Ang)-aldosterone system (RAAS). We hypothesized that ANCS exposure alters the RAAS in adolescents born prematurely.

Published
2017
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88. Regulation of Cardiovascular Control Mechanisms by Angiotensin-(1–7) and Angiotensin-Converting Enzyme 2

Author

Ferrario, Carlos M., Averill, David B., Brosnihan, K. Bridget, Chappell, Mark C., Diz, Debra I., Gallagher, Patricia E., Neves, Liomar, and Tallant, E. Ann

Subjects
Afferent Arteriole, Bovine Aortic Endothelial Cell, Severe Acute Respiratory Syndrome, Proximal Tubule, hormones, hormone substitutes, and hormone antagonists, Article
Abstract

Among the molecular forms of angiotensin peptides generated by the action of renin on angiotensinogen (Aogen), both angiotensin II (Ang II) and the amino terminal heptapeptide angiotensin-(1–7) [Ang-(1–7)] are critically involved in the long-term control of tissue perfusion, cell-cell communication, development, and growth. Whereas an impressive body of literature continues to uncover pleiotropic effects of Ang II in the regulation of cell function, research on Ang-(1–7) has a shorter history as it was only 16 yr ago that a biological function for this heptapeptide was first demonstrated in the isolated rat neuro-hypophysial explant preparation (1). On the contrary, the synthesis of angiotonin/ hypertensin (now Ang II) was first obtained in 1957 (2), three decades ahead of the discovery of Ang-(1–7) biological properties.

Published
2010

92. Effects of supervised exercise and dietary nitrate in older adults with controlled hypertension and/or heart failure with preserved ejection fraction

Author

Shaltout, Hossam A., primary, Eggebeen, Joel, additional, Marsh, Anthony P., additional, Brubaker, Peter H., additional, Laurienti, Paul J., additional, Burdette, Jonathan H., additional, Basu, Swati, additional, Morgan, Ashley, additional, Dos Santos, Patricia C., additional, Norris, James L., additional, Morgan, Timothy M., additional, Miller, Gary D., additional, Rejeski, W. Jack, additional, Hawfield, Amret T., additional, Diz, Debra I., additional, Becton, J. Thomas, additional, Kim-Shapiro, Daniel B., additional, and Kitzman, Dalane W., additional

Published
2017
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95. Why publish in the American Journal of Physiology-Heart and Circulatory Physiology?

Author

Zucker, Irving H., primary, Lindsey, Merry L., additional, Delmar, Mario, additional, De Windt, Leon J., additional, Des Rosiers, Christine, additional, Diz, Debra I., additional, Hester, Robert L., additional, Jones, Steven P., additional, Kanagy, Nancy L., additional, Kitakaze, Masafumi, additional, Liao, Ronglih, additional, Lopaschuk, Gary D., additional, Patel, Kaushik P., additional, Recchia, Fabio A., additional, Sadoshima, Junichi, additional, Shah, Ajay M., additional, Ungvari, Zoltan, additional, Benjamin, Ivor J., additional, Blaustein, Mordecai P., additional, Charkoudian, Nisha, additional, Efimov, Igor R., additional, Gutterman, David, additional, Kass, David A., additional, Liao, Yulin, additional, O'Leary, Donal S., additional, Ripplinger, Crystal M., additional, and Wolin, Michael S., additional

Published
2017
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100. Pathways for angiotensin-(1--7) metabolism in pulmonary and renal tissues

Author

ALLRED, ALICIA J., DIZ, DEBRA I., FERRARIO, CARLOS M., and CHAPPELL, MARK C.

Subjects
Angiotensin -- Physiological aspects, Angiotensin converting enzyme -- Physiological aspects, Aminopeptidases -- Physiological aspects, Lisinopril -- Physiological aspects, Biological sciences
Abstract

Allred, Alicia J., Debra I. Diz, Carlos M. Ferwario, and Mark C. Chappell. Pathways for angiotensin-(1--7) metabolism in pulmonary and renal tissues. Am J Physiol Renal Physiol 279: F841-F850, 2000.--Two of the primary sites of actions for angiotensin (ANG)-(1-7) are the vasculature and the kidney. Because little information exists concerning the metabolism of ANG-(1-7) in these tissues, we investigated the hydrolysis of the peptide in rat lung and renal brush-border membrane (BBM) preparations. Radiolabeled ANG-(1-7) was hydrolyzed primarily to ANG-(1-5) by pulmonary membranes. The ANG-converting enzyme (ACE) inhibitor lisinopril abolished the generation of ANG-(1-5), as well as that of smaller metabolites. Kinetic studies of the hydrolysis of ANG-(1-7) to ANG-(1-5) by somatic (pulmonary) and germinal (testes) forms of rat ACE yielded similar values, suggesting that the COOH-domain is responsible for the hydrolysis of ANG-(1-7). Pulmonary metabolism of ANG-(1-5) yielded ANG-(3-5) and was independent of ACE but may involve peptidyl or dipeptidyl aminopeptidases. In renal cortex BBM, ANG-(1-7) was rapidly hydrolyzed to mono- and dipeptide fragments and ANG-(1-4). Aminopeptidase (AP) inhibition attenuated the hydrolysis of ANG-(1-7) and increased ANG-(1-4) formation. Combined treatment with AP and neprilysin (Nep) inhibitors abolished ANG-(1-4) formation and preserved ANG-(1-7). ACE inhibition had no effect on the rate of hydrolysis or the metabolites formed in the BBM. In conclusion, ACE was the major enzymatic activity responsible for the metabolism of ANG-(1-7) in the lung, which is consistent with the ability of ACE inhibitors to increase the half-life of circulating ANG-(1-7) and raise endogenous levels of the peptide. An alternate pathway of metabolism was revealed in the renal cortex, where increased AP and Nep activities, relative to ACE activity, promote conversion of ANG-(1-7) to ANG-(1-4) and smaller fragments. angiotensin-converting enzyme; neprilysin; lisinopril; SCH-39370; aminopeptidase; amastatin

Published
2000

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