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—This  study was conducted to determine potentially differential effects  between an angiotensin II type 1  (AT1 ) receptor antagonist and an ACE  inhibitor on systemic, renal, and glomerular  hemodynamics and pathological changes in spontaneously  hypertensive rats (SHR) withN ω -nitro-l &gt;-arginine  methyl ester (L-NAME)–exacerbated nephrosclerosis. The  hemodynamic, renal micropuncture, and pathological  studies were performed in 9 groups of 17-week-old male SHR treated as  follows: group 1, controls (n=16); group 2, candesartan (10 mg/kg per  day for 3 weeks) (n=7); group 3, enalapril (30 mg/kg per day for 3  weeks) (n=8); group 4, candesartan (5 mg/kg per day) plus enalapril (15  mg/kg per day for 3 weeks) (n=9); group 5, L-NAME (50 mg/L in drinking  water for 3 weeks) (n=17); group 6, L-NAME (50 mg/L) plus candesartan  (10 mg/kg per day for 3 weeks) (n=7); group 7, L-NAME (50 mg/L) for 3  weeks followed by candesartan (10 mg/kg per day) for another 3 weeks  (n=8); group 8, L-NAME (50 mg/L) plus enalapril (30 mg/kg per day for 3  weeks) (n=7); and group 9, L-NAME (50 mg/L) plus enalapril (30 mg/kg  per day) and the bradykinin antagonist icatibant (500  μg/kg SC per day via osmotic minipump for 3 weeks) (n=7). Both  candesartan and enalapril similarly reduced mean arterial  pressure and total peripheral resistance index. These  changes were associated with significant decreases in afferent and  efferent glomerular arteriolar resistances as well as  glomerular capillary pressure. Histopathologically, the  glomerular and arterial injury scores were  decreased significantly, and left ventricular and aortic  masses also were diminished significantly in all treated groups.  L-NAME–induced urinary protein excretion was prevented by both  candesartan and enalapril. Thus, both AT1 receptor and ACE inhibition prevented and reversed the  pathophysiological alterations of  L-NAME–exacerbated nephrosclerosis in SHR. Itatibant  only blunted the antihypertensive effects of enalapril but did not  attenuate the beneficial effects of ACE inhibition on the  L-NAME–induced nephrosclerosis. Thus, the  AT1 receptor antagonism and ACE inhibition have  similar renal preventive effects, which most likely were achieved  through reduction in the effects of angiotensin II, and ACE  inhibition of bradykinin degradation demonstrated little evidence of  renoprotection.

hypertension

Angiotensin Type 1 Receptor Antagonism and ACE Inhibition Produce Similar Renoprotection in N ω -Nitro- <scp>l</scp> &gt;-Arginine Methyl Ester/Spontaneously Hypertensive Rats

Angiotensin Type 1 Receptor Antagonism and ACE Inhibition Produce Similar Renoprotection in N ω -Nitro- l >-Arginine Methyl Ester/Spontaneously Hypertensive Rats

Angiotensin Type 1 Receptor Antagonism and ACE Inhibition Produce Similar Renoprotection in N ^ω -Nitro- l >-Arginine Methyl Ester/Spontaneously Hypertensive Rats