scholarly journals Role of the renal sympathetic nerves in renal sodium/potassium handling and renal damage in spontaneously hypertensive rats

2016 ◽  
Vol 12 (4) ◽  
pp. 2547-2553 ◽  
Author(s):  
Jianling Li ◽  
Qiaoling He ◽  
Weifeng Wu ◽  
Qingjie Li ◽  
Rongjie Huang ◽  
...  
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Renal Damage ◽  
Sympathetic Nerves ◽  
Hypertensive Rats ◽  
Sodium Potassium ◽  
Spontaneously Hypertensive ◽  
Renal Sympathetic

Cardiovascular effects of prorenin blockade in genetically spontaneously hypertensive rats on normal and high-salt diet

2008 ◽  
Vol 295 (3) ◽  
pp. H1117-H1121 ◽  
Author(s):  
Dinko Susic ◽  
Xiaoyan Zhou ◽  
Edward D. Frohlich ◽  
Howard Lippton ◽  
Martha Knight
Keyword(s):  
Arterial Pressure ◽  
Left Ventricular Function ◽  
Ventricular Function ◽  
Spontaneously Hypertensive Rats ◽  
Renal Damage ◽  
Left Ventricular ◽  
Normal Diet ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive

Recent reports have demonstrated a potential role of tissue prorenin in the pathogenesis of cardiovascular and renal damage. This study was designed to examine the role of prorenin in the pathogenesis of target organ damage in spontaneously hypertensive rats (SHRs), the best naturally occurring experimental model of essential hypertension. To this end, we studied 20-wk-old male SHRs receiving a normal diet and 8-wk-old male SHRs given food with 8% NaCl. One-half the rats in each group were given prorenin inhibitor (PRAM-1, 0.1 mg·kg−1·day−1) via osmotic minipumps; the other half served as controls. Arterial pressure, left ventricular function, cardiovascular mass indexes, cardiac fibrosis, and renal function were examined at the end of the experiment. Arterial pressure was unaffected by PRAM-1 in rats on either regular or salt-excess diets. In those rats receiving a normal diet, the blockade of prorenin activation consistently reduced left ventricular mass but affected no other variable. Salt-loaded rats given PRAM-1 for 8 wk demonstrated ( 1) reduced serum creatinine level, ( 2) decreased left ventricular mass, ( 3) improved left ventricular function, and ( 4) reduced left ventricular fibrosis. These data demonstrated that the blockade of nonproteolytic activation of prorenin exerted significant cardiovascular and renal benefit in SHRs with cardiovascular damage produced by salt excess and suggested that the activation of cardiovascular or renal prorenin may be a major mechanism that mediates cardiac and renal damage in this form of accelerated hypertension.

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