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191 results on '"Sanada, Hironobu"'

1. G Protein-Coupled Receptor Kinase 4 Gene Variants in Human Essential Hypertension

Author

Felder, Robin A., Sanada, Hironobu, Xu, Jing, Yu, Pei-Ying, Wang, Zheng, Watanabe, Hidetsuna, Asico, Laureano D., Wang, Wei, Zheng, Shaopeng, Yamaguchi, Ikuyo, Williams, Scott M., Gainer, James, Brown, Nancy J., Hazen-Martin, Debra, Wong, Lee-Jun C., Robillard, Jean E., Carey, Robert M., Eisner, Gilbert M., and Jose, Pedro A.

Published
2002

11. Angiotensin II type 1 receptor blocker attenuates the activation of ERK and NADPH oxidase by mechanical strain in mesangial cells in the absence of angiotensin II

Author

Yatabe, Junichi, Sanada, Hironobu, Yatabe, Midori Sasaki, Hashimoto, Shigeatsu, Yoneda, Minoru, Felder, Robin A., Jose, Pedro A., and Watanabe, Tsuyoshi

Subjects
Angiotensin -- Physiological aspects, Angiotensin -- Research, Protein kinases -- Physiological aspects, Protein kinases -- Research, Kidney diseases -- Risk factors, Kidney diseases -- Prevention, Kidney diseases -- Research, Biological sciences
Abstract

It has been reported that mechanical strain activates extracellular signal-regulated protein kinases (ERK) without the involvement of angiotensin II (Ang II) in cardiomyocytes. We examined the effects of mechanical strain on ERK phosphorylation levels in the absence of Ang II using rat mesangial cells. The ratio of phosphorylated ERK (p-ERK) to total ERK expression was increased by cyclic mechanical strain in a timeand elongation strength-dependent manner. With olmesartan [Ang II type 1 receptor (AT1R) antagonist] pretreatment, p-ERK plateau levels decreased in a dose-dependent manner (E[C.sub.50] = 1.3 x [10.sup.-8] M, maximal inhibition 50.6 [+ or -] 11.0% at [10.sup.-5] M); a similar effect was observed with RNA interference against Ang II type I A receptor (A[T.sub.1A]R) and Tempol, a superoxide dismutase mimetic. In addition to the inhibition of p-ERK levels, olmesartan blocked the increase in cell surface and phosphorylated [p47.sup.phox] induced by mechanical strain and also lowered the mRNA expression levels of NADPH oxidase subunits. These results demonstrate that mechanical strain stimulates AT1R to phosphorylate ERK in mesangial cells in the absence of Ang II. This mechanotransduction mechanism is involved in the oxidative stress caused by NADPH oxidase and is blocked by olmesartan. The inverse agonistic activity of this AT1R blocker may be useful for the prevention of mesangial proliferation and renal damage caused by mechanical strain/oxidative stress regardless of circulating or tissue Ang II levels. hypertension

Published
2009

16. Effects of a high-sodium diet on renal tubule Ca2+ transporter and claudin expression in Wistar-Kyoto rats

Author

Yatabe Midori Sasaki, Yatabe Junichi, Takano Kozue, Murakami Yuta, Sakuta Rina, Abe Sadahiko, Sanada Hironobu, Kimura Junko, and Watanabe Tsuyoshi

Subjects
Calcium, Sodium chloride, Distal tubule, Na+/Ca2+ exchanger, Ca2+ channel, Claudins, Diseases of the genitourinary system. Urology, RC870-923
Abstract

Abstract Background Urinary Ca2+ excretion increases with dietary NaCl. NaCl-induced calciuria may be associated with hypertension, urinary stone formation and osteoporosis, but its mechanism and long-term effects are not fully understood. This study examined alterations in the expressions of renal Ca2+ transporters, channels and claudins upon salt loading to better understand the mechanism of salt-induced urinary Ca2+ loss. Methods Eight-week old Wistar-Kyoto rats were fed either 0.3% or 8% NaCl diet for 8 weeks. Renal cortical expressions of Na+/Ca2+ exchanger 1 (NCX1), Ca2+ pump (PCMA1b), Ca2+ channel (TRPV5), calbindin-D28k, and claudins (CLDN-2, -7, -8, -16 and −19) were analyzed by quantitative PCR, western blot and/or immunohistochemistry. Results Fractional excretion of Ca2+ increased 6.0 fold with high-salt diet. Renal cortical claudin-2 protein decreased by approximately 20% with decreased immunological staining on tissue sections. Claudin-16 and −19 expressions were not altered. Renal cortical TRPV5, calbindin-D28k and NCX1 expressions increased 1.6, 1.5 and 1.2 fold, respectively. Conclusions Chronic high-salt diet decreased claudin-2 protein and increased renal TRPV5, calbindin-D28k, and NCX1. Salt loading is known to reduce the proximal tubular reabsorption of both Na+ and Ca2+. The reduction in claudin-2 protein expression may be partly responsible for the reduced Ca2+ reabsorption in this segment. The concerted upregulation of more distal Ca2+-transporting molecules may be a physiological response to curtail the loss of Ca2+, although the magnitude of compensation does not seem adequate to bring the urinary Ca2+ excretion down to that of the normal-diet group.

Published
2012
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17. HUMAN GRK4γ142V VARIANT PROMOTES AT1R-MEDIATED HYPERTENSION VIA RENAL HDAC1 INHIBITION

Author

Wang, Zheng, Zeng, Chunyu, Villar, Van Anthony M., Chen, Shi-You, Konkalmatt, Prasad, Wang, Xiaoyan, Asico, Laureano D., Jones, John E., Yang, Yu, Sanada, Hironobu, Felder, Robin A., Eisner, Gilbert M., Weir, Matthew R., Armando, Ines, and Jose, Pedro A.

Subjects
Male, G-Protein-Coupled Receptor Kinase 4, Immunoblotting, Tetrazoles, Blood Pressure, Histone Deacetylase 1, Mice, Transgenic, Kidney, Real-Time Polymerase Chain Reaction, Article, Receptor, Angiotensin, Type 1, Mice, Animals, Humans, Reverse Transcriptase Polymerase Chain Reaction, Biphenyl Compounds, Mice, Inbred C57BL, Disease Models, Animal, HEK293 Cells, Gene Expression Regulation, Hypertension, RNA, Benzimidazoles, Female, Essential Hypertension, Angiotensin II Type 1 Receptor Blockers
Abstract

The influence of a single gene on the pathogenesis of essential hypertension may be difficult to ascertain, unless the gene interacts with other genes that are germane to blood pressure regulation. G-protein-coupled receptor kinase type 4 (GRK4) is one such gene. We have reported that the expression of its variant hGRK4γ(142V) in mice results in hypertension because of impaired dopamine D1 receptor. Signaling through dopamine D1 receptor and angiotensin II type I receptor (AT1R) reciprocally modulates renal sodium excretion and blood pressure. Here, we demonstrate the ability of the hGRK4γ(142V) to increase the expression and activity of the AT1R. We show that hGRK4γ(142V) phosphorylates histone deacetylase type 1 and promotes its nuclear export to the cytoplasm, resulting in increased AT1R expression and greater pressor response to angiotensin II. AT1R blockade and the deletion of the Agtr1a gene normalize the hypertension in hGRK4γ(142V) mice. These findings illustrate the unique role of GRK4 by targeting receptors with opposite physiological activity for the same goal of maintaining blood pressure homeostasis, and thus making the GRK4 a relevant therapeutic target to control blood pressure.

Published
2015

19. Urinary Sodium-to-Potassium Ratio Tracks the Changes in Salt Intake during an Experimental Feeding Study Using Standardized Low-Salt and High-Salt Meals among Healthy Japanese Volunteers

Author

Yatabe, Midori, primary, Iwahori, Toshiyuki, additional, Watanabe, Ami, additional, Takano, Kozue, additional, Sanada, Hironobu, additional, Watanabe, Tsuyoshi, additional, Ichihara, Atsuhiro, additional, Felder, Robin, additional, Miura, Katsuyuki, additional, Ueshima, Hirotsugu, additional, Kimura, Junko, additional, and Yatabe, Junichi, additional

Published
2017
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21. Human GRK4γ142VVariant Promotes Angiotensin II Type I Receptor–Mediated Hypertension via Renal Histone Deacetylase Type 1 Inhibition

Author

Wang, Zheng, primary, Zeng, Chunyu, additional, Villar, Van Anthony M., additional, Chen, Shi-You, additional, Konkalmatt, Prasad, additional, Wang, Xiaoyan, additional, Asico, Laureano D., additional, Jones, John E., additional, Yang, Yu, additional, Sanada, Hironobu, additional, Felder, Robin A., additional, Eisner, Gilbert M., additional, Weir, Matthew R., additional, Armando, Ines, additional, and Jose, Pedro A., additional

Published
2016
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23. Association Between Serum Uric Acid Levels/Hyperuricemia and Hypertension Among 85,286 Japanese Workers

Author

Yokokawa, Hirohide, primary, Fukuda, Hiroshi, additional, Suzuki, Akihito, additional, Fujibayashi, Kazutoshi, additional, Naito, Toshio, additional, Uehara, Yuki, additional, Nakayama, Akiyoshi, additional, Matsuo, Hirotaka, additional, Sanada, Hironobu, additional, Jose, Pedro A., additional, Miwa, Yuichi, additional, Hisaoka, Teruhiko, additional, and Isonuma, Hiroshi, additional

Published
2015
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28. Mini Nutritional Assessment as a useful method to predict the development of pressure ulcer among elderly inpatients

Author

Yatabe, Midori Sasaki, Taguchi, Fumie, Ishida, Izumi, Sato, Atsuko, Kameda, Toshio, Ueno, Shuichi, Takano, Kozue, Watanabe, Tsuyoshi, Sanada, Hironobu, Yatabe, Junichi, Yatabe, Midori Sasaki, Taguchi, Fumie, Ishida, Izumi, Sato, Atsuko, Kameda, Toshio, Ueno, Shuichi, Takano, Kozue, Watanabe, Tsuyoshi, Sanada, Hironobu, and Yatabe, Junichi

Abstract

type:Text, Author Manuscript (Submitted version), OBJECTIVES: Malnutrition is a major risk factor of pressure ulcers (PU). However, the best method of nutritional assessment to prevent PU is still unclear. This study was designed to determine the usefulness of Mini Nutritional Assessment (MNA) and plasma amino acid analysis to predict the formation of PU among inpatients. DESIGN: This was a prospective, observational cohort study with a mean observation period of 62.2±86.4 days. SETTING: Intermediate and acute care wards of a hospital in rural Japan. PARTICIPANTS: The 422 patients analyzed had an average age of 85.0±7.6 years. MEASUREMENTS: MNA, Subjective Global Assessment (SGA), Braden Scale (PU prognostic score), pressure ulcer formation, and biochemical analysis including plasma amino acid concentrations. RESULTS: PU developed in 7.1% of the patients. A MNA score of less than 8 was more sensitive than a rating of moderate or severe malnourishment on the SGA combined with a Braden Scale score of <15 in predicting future PU. Area under the receiver operating characteristic curve (AUC) of MNA was superior to that of the Braden Scale. Braden Scale nutrition subscore had the lowest AUC among the six Braden Scale subscores. The PU group showed significantly lower plasma arginine concentrations than the No PU group. CONCLUSION: MNA was able to predict the development of PU. A MNA of <8 performed better than the SGA, Braden Scale, and plasma arginine levels in predicting PU development. Although lower plasma arginine concentration at time of admission was associated with PU development, the area under the ROC curve was not significant. The findings from this prospective study support the use of nutritional assessment among inpatients in order to predict PU risk and target appropriate interventions.

Published
2013

30. Effects of a high-sodium diet on renal tubule Ca2+ transporter and claudin expression in Wistar-Kyoto rats

Author

Yatabe, Midori Sasaki, Yatabe, Junichi, Takano, Kozue, Murakami, Yuta, Sakuta, Rina, Abe, Sadahiko, Sanada, Hironobu, Kimura, Junko, Watanabe, Tsuyoshi, Yatabe, Midori Sasaki, Yatabe, Junichi, Takano, Kozue, Murakami, Yuta, Sakuta, Rina, Abe, Sadahiko, Sanada, Hironobu, Kimura, Junko, and Watanabe, Tsuyoshi

Abstract

type:Text, Background: Urinary Ca^{2+} excretion increases with dietary NaCl. NaCl-induced calciuria may be associated with hypertension, urinary stone formation and osteoporosis, but its mechanism and long-term effects are not fully understood. This study examined alterations in the expressions of renal Ca^{2+} transporters, channels and claudins upon salt loading to better understand the mechanism of salt-induced urinary Ca^{2+} loss. Methods: Eight-week old Wistar-Kyoto rats were fed either 0.3% or 8% NaCl diet for 8 weeks. Renal cortical expressions of Na+/Ca2+ exchanger 1 (NCX1), Ca^{2+} pump (PCMA1b), Ca^{2+} channel (TRPV5), calbindin-D28k, and claudins (CLDN-2, -7, -8, -16 and −19) were analyzed by quantitative PCR, western blot and/or immunohistochemistry. Results: Fractional excretion of Ca^{2+} increased 6.0 fold with high-salt diet. Renal cortical claudin-2 protein decreased by approximately 20% with decreased immunological staining on tissue sections. Claudin-16 and −19 expressions were not altered. Renal cortical TRPV5, calbindin-D28k and NCX1 expressions increased 1.6, 1.5 and 1.2 fold, respectively. Conclusions: Chronic high-salt diet decreased claudin-2 protein and increased renal TRPV5, calbindin-D28k, and NCX1. Salt loading is known to reduce the proximal tubular reabsorption of both Na+ and Ca^{2+}. The reduction in claudin-2 protein expression may be partly responsible for the reduced Ca^{2+} reabsorption in this segment. The concerted upregulation of more distal Ca^{2+}-transporting molecules may be a physiological response to curtail the loss of Ca^{2+}, although the magnitude of compensation does not seem adequate to bring the urinary Ca^{2+} excretion down to that of the normal-diet group.

Published
2012

31. Abstract 52: Human Grk4γ142v, Via Histone Deacetylase 1, Produces At1r-dependent Hypertension

Author

Jose, Pedro, primary, Wang, Zheng, additional, Sanada, Hironobu, additional, Yoneda, Minoru, additional, Zheng, Chnuyu, additional, Williams, Scott, additional, Bartlett, Jacqueline, additional, White, Marquitta, additional, Gordon, Lindsay, additional, Liu, Monica, additional, Konkalmatt, Prasad, additional, Wang, Xiaoyan, additional, Asico, Laureano, additional, Villar, Van Anthony, additional, Jones, John, additional, Armando, Ines, additional, Felder, Robin, additional, and Eisner, Gilbert, additional

Published
2013
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32. Association Between Serum Uric Acid Levels/Hyperuricemia and Hypertension Among 85,286 Japanese Workers.

Author

Yokokawa, Hirohide, Fukuda, Hiroshi, Suzuki, Akihito, Fujibayashi, Kazutoshi, Naito, Toshio, Uehara, Yuki, Nakayama, Akiyoshi, Matsuo, Hirotaka, Sanada, Hironobu, Jose, Pedro A., Miwa, Yuichi, Hisaoka, Teruhiko, and Isonuma, Hiroshi

Subjects
HYPERTENSION epidemiology, BLOOD pressure, EMPLOYMENT, HYPERTENSION, HYPERURICEMIA, SEX distribution, URIC acid, BODY mass index, DISEASE prevalence, GOUT suppressants, CROSS-sectional method, THERAPEUTICS
Abstract

This cross-sectional study from January 2012 to December 2012 aimed to examine the sex-specific association between serum uric acid (SUA) levels/hyperuricemia and hypertension among Japanese patients. SUA level, medical histories, and lifestyle-related items were collected from 85,286 of 136,770 participants. Among those with hyperuricemia, the median age was 46 years and 97% were men, which was significantly different than those without hyperurecemia (44 years and 56%, respectively; P<.01). Hyperuricemia was 1.79 times more likely in hypertensive men than normotensive men and almost six times more likely in hypertensive women (odds ratio=5.92 and adjusted odds ratio=1.33 for men and adjusted odds ratio=1.81 for women) after multivariate analysis. SUA quartiles positively correlated with systolic and diastolic blood pressures in both sexes. Hyperuricemia and SUA levels were significantly associated with hypertension in both sexes. These findings underscore the importance of maintaining normal SUA levels to manage and prevent hypertension. Better management of SUA as well as blood pressure may have potential in preventing future cardiovascular disorders. [ABSTRACT FROM AUTHOR]

Published
2016
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34. Novel role of sorting nexin 5 in renal D 1 dopamine receptor trafficking and function: implications for hypertension

Author

Villar, Van Anthony M., primary, Armando, Ines, additional, Sanada, Hironobu, additional, Frazer, Lauren C., additional, Russo, Christen M., additional, Notario, Patricia M., additional, Lee, Hewang, additional, Comisky, Lauren, additional, Russell, Holly Ann, additional, Yang, Yu, additional, Jurgens, Julie A., additional, Jose, Pedro A., additional, and Jones, John E., additional

Published
2012
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44. Amelioration of Genetic Hypertension by Suppression of Renal G Protein–Coupled Receptor Kinase Type 4 Expression

Author

Sanada, Hironobu, primary, Yatabe, Junichi, additional, Midorikawa, Sanae, additional, Katoh, Tetsuo, additional, Hashimoto, Shigeatsu, additional, Watanabe, Tsuyoshi, additional, Xu, Jing, additional, Luo, Yingjin, additional, Wang, Xiaoyan, additional, Zeng, Chunyu, additional, Armando, Ines, additional, Felder, Robin A., additional, and Jose, Pedro A., additional

Published
2006
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45. Single-Nucleotide Polymorphisms for Diagnosis of Salt-Sensitive Hypertension

Author

Sanada, Hironobu, primary, Yatabe, Junichi, primary, Midorikawa, Sanae, primary, Hashimoto, Shigeatsu, primary, Watanabe, Tsuyoshi, primary, Moore, Jason H, primary, Ritchie, Marylyn D, primary, Williams, Scott M, primary, Pezzullo, John C, primary, Sasaki, Midori, primary, Eisner, Gilbert M, primary, Jose, Pedro A, primary, and Felder, Robin A, primary

Published
2006
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46. Differential Effects of Angiotensin II Type-1 Receptor Antisense Oligonucleotides on Renal Function in Spontaneously Hypertensive Rats

Author

Yoneda, Minoru, primary, Sanada, Hironobu, additional, Yatabe, Junichi, additional, Midorikawa, Sanae, additional, Hashimoto, Shigeatsu, additional, Sasaki, Midori, additional, Katoh, Tetsuo, additional, Watanabe, Tsuyoshi, additional, Andrews, Peter M., additional, Jose, Pedro A., additional, and Felder, Robin A., additional

Published
2005
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