scholarly journals Effects of Renin-Angiotensin System Inhibitors on Renal Expression of Renalase in Sprague-Dawley Rats Fed With High Salt Diet

2015 ◽  
Vol 40 (6) ◽  
pp. 605-613 ◽  
Author(s):  
Yang Wang ◽  
Bing-Qing Xie ◽  
Wei-Hua Gao ◽  
Ding-Yi Yan ◽  
Wen-Ling Zheng ◽  
...  
2017 ◽  
Vol 6 (1) ◽  
pp. 29 ◽  
Author(s):  
Gabriel Cao ◽  
Silvana Lorena Della Penna ◽  
Nicolás Martín Kouyoumdzian ◽  
Marcelo Roberto Choi ◽  
Susana Gorzalczany ◽  
...  

2018 ◽  
Vol 36 (12) ◽  
pp. 2369-2379 ◽  
Author(s):  
Yanping Liu ◽  
Linglu Qi ◽  
Jue Wu ◽  
Ting Xu ◽  
Chunli Yang ◽  
...  

2011 ◽  
Vol 29 (12) ◽  
pp. 2454-2461 ◽  
Author(s):  
Norman K. Hollenberg ◽  
Naomi D.L. Fisher ◽  
Juerg Nussberger ◽  
George V. Moukarbel ◽  
Ebrahim Barkoudah ◽  
...  

2011 ◽  
Vol 34 (1) ◽  
pp. 1-11 ◽  
Author(s):  
I. Drenjančević-Perić ◽  
B. Jelaković ◽  
J.H. Lombard ◽  
M.P. Kunert ◽  
A. Kibel ◽  
...  

2010 ◽  
Vol 12 (11) ◽  
pp. 1171-1178 ◽  
Author(s):  
Philippe Le Corvoisier ◽  
Christophe Adamy ◽  
Lucien Sambin ◽  
Bertrand Crozatier ◽  
Alain Berdeaux ◽  
...  

2002 ◽  
Vol 92 (2) ◽  
pp. 627-633 ◽  
Author(s):  
Eugene C. Fletcher ◽  
Natalia Orolinova ◽  
Michael Bader

By using an inspired oxygen fraction that produces oxyhemoglobin desaturation equivalent to that seen in human sleep apnea, we have demonstrated that 35 days of recurrent episodic hypoxia (every 30 s for 7 h/day) results in an 8–13 mmHg persistent increase in diurnal systemic mean arterial blood pressure (MAP) in rats. Blockade of angiotensin II receptors (AT1a) eliminates this response. Separate groups of male Sprague-Dawley rats were fed high-salt (8%), ad libitum-salt, or low-salt (0.1%) diets for 7 wk: 2 wk of wash-in for baseline blood pressure measurement and 5 wk of experimental conditions. Rats in each salt group were subjected to episodic hypoxia whereas controls remained unhandled under normoxic conditions. MAP remained at basal levels in all nonepisodic hypoxia controls as well as high-salt-diet episodic hypoxia-exposed rats. Ad lib and low-salt episodic hypoxia rats showed an increase in MAP from 106 and 104 mmHg at baseline to 112 and 113 mmHg, respectively ( P < 0.05). Whole kidney renin mRNA was suppressed in high-salt controls and episodic hypoxia rats, whereas kidney AT1a mRNA showed opposite changes. Suppression of the renin-angiotensin system with a high-salt diet blocks the increase in MAP in episodic hypoxia-challenged rats, in part by suppressing local tissue renin levels. Upregulation of the tissue angiotensin II system appears to be necessary for the chronic blood pressure changes that occur from episodic hypoxia.


2002 ◽  
Vol 283 (1) ◽  
pp. R243-R248 ◽  
Author(s):  
Jennifer M. Sasser ◽  
Jennifer S. Pollock ◽  
David M. Pollock

To determine the influence of chronic ANG II infusion on urinary, plasma, and renal tissue levels of immunoreactive endothelin (ET), ANG II (65 ng/min) or saline vehicle was delivered via osmotic minipump in male Sprague-Dawley rats given either a high-salt diet (10% NaCl) or normal-salt diet (0.8% NaCl). High-salt diet alone caused a slight but not statistically significant increase (7 ± 1%) in mean arterial pressure (MAP). MAP was significantly increased in ANG II-infused rats (41 ± 10%), and the increase in MAP was significantly greater in ANG II rats given a high-salt diet (59 ± 1%) compared with the increase observed in rats given a high-salt diet alone or ANG II infusion and normal-salt diet. After a 2-wk treatment, urinary excretion of immunoreactive ET was significantly increased by ∼50% in ANG II-infused animals and by over 250% in rats on high-salt diet, with or without ANG II infusion. ANG II infusion combined with high-salt diet significantly increased immunoreactive ET content in the cortex and outer medulla, but this effect was not observed in other groups. In contrast, high-salt diet, with or without ANG II infusion, significantly decreased immunoreactive ET content within the inner medulla. These data indicate that chronic elevations in ANG II levels and sodium intake differentially affect ET levels within the kidney and provide further support for the hypothesis that the hypertensive effects of ANG II may be due to interaction with the renal ET system.


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