THE ROLE OF NITRIC-OXIDE IN ANGIOTENSIN-II-INDUCED RENAL VASOCONSTRICTION IN RENOVASCULAR HYPERTENSION

Objective To evaluate the contribution of nitric oxide to the regulati on of angiotensin II-induced renal vasoconstriction in normotensive ra ts and in rats with aortic coarctation-induced hypertension. Methods W e evaluated the renal vascular reactivity of nonischemic kidney to ang iotensin II with and without nitric oxide synthesis inhibitor (N-G-nit ro-L-arginine methyl ester) in the isolated perfused kidney. The nitri te concentration in renal perfusate of nonischemic kidney was measured as an index of nitric oxide released and the activity of nitric oxide synthase in renal tissue was determined by production of [H-3]-L-citr ulline. Results The perfusion of N-G-nitro-L-arginine methyl ester pot entiated angiotensin II-induced renal vasoconstriction in normotensive rats but had no effect on hypertensive rats. The release of nitrites in kidneys from hypertensive rats was lower than that in kidneys from normotensive rats, The activity of renal nitric oxide synthase was les s in the hypertensive rats than it was in the normotensive rats. Concl usions Nitric oxide counteracts the vasoconstrictor effect of angioten sin II in normotensive rats, whereas this protective mechanism is impa ired in hypertensive rats. This impairment potentiates effect of angio tensin II on vascular resistance, thereby contributing to the developm ent of high blood pressure. (C) 1998 Lippincott-Raven Publishers.