Renal Nitric Oxide and Angiotensin II Interaction in Renovascular Hypertension

• Published in: Hypertension (Dallas, Tex. 1979) Tex. 1979), 1993-08, Vol.22 (2), p.237-242
• Main Authors: Sigmon, David H, Beierwaltes, William H
• Format: Article
• Language: English
• Subjects: Angiotensin II - metabolism; Animals; Antihypertensive Agents - pharmacology; Arginine - analogs & derivatives; Arginine - pharmacology; Arterial hypertension. Arterial hypotension; Biological and medical sciences; Biphenyl Compounds - pharmacology; Blood and lymphatic vessels; Cardiology. Vascular system; Endothelium, Vascular - metabolism; Experimental diseases; Hemodynamics - drug effects; Hypertension, Renovascular - metabolism; Imidazoles - pharmacology; Kidney - metabolism; Losartan; Male; Medical sciences; NG-Nitroarginine Methyl Ester; Nitric Oxide - antagonists & inhibitors; Nitric Oxide - metabolism; Rats; Rats, Sprague-Dawley; Renal Circulation - drug effects; Tetrazoles - pharmacology
• ISSN: 0194-911X; 1524-4563
• DOI: 10.1161/01.HYP.22.2.237

In two-kidney, one clip (2K1C) renovascular hypertension, blood flow is reduced to the clipped but not to the nonclipped kidney, despite elevated angiotensin II. To determine possible interactions between endothelium-derived nitric oxide and angiotensin, we studied bilateral renal blood flow using radioactive microspheres in anesthetized 2K1C hypertensive rats 4 weeks after clipping. We studied the response to nitric oxide synthesis inhibition with 10 mg/kg body wt N-nitro-L-arginine-methyl ester (L-NAME) in hypertensive rats untreated (n=5) or treated (n=5) with 10 mg/kg body wt of the angiotensin II antagonist losartan. 2K1C rats had a blood pressure of 159±9 mm Hg, and renal blood flow to the clipped kidney was reduced 87% compared with the nonclipped kidney. L-NAME increased blood pressure 36±5 mm Hg and decreased renal blood flow in the nonclipped kidney 61% (4.9±0.5 to 1.9±0.4 mL/min per gram kidney weight, P