Objective: To evaluate the contribution of nitric oxide to the regulation of angiotensin II-induced renal vasoconstriction in normotensive rats and in rats with aortic coarctation-induced hypertension.
Methods: We evaluated the renal vascular reactivity of nonischemic kidney to angiotensin II with and without nitric oxide synthesis inhibitor (NG-nitro-L-arginine methyl ester) in the isolated perfused kidney. The nitrite 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 [3H]-L-citrulline.
Results: The perfusion of NG-nitro-L-arginine methyl ester potentiated 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 less in the hypertensive rats than it was in the normotensive rats.
Conclusions: Nitric oxide counteracts the vasoconstrictor effect of angiotensin II in normotensive rats, whereas this protective mechanism is impaired in hypertensive rats. This impairment potentiates effect of angiotensin II on vascular resistance, thereby contributing to the development of high blood pressure.