[Role of nitric oxide in the modulation of the vascular response to angiotensin II in hypertensive rats].

Vasorelaxant activity induced by nitric oxide has been associated with a regulator activity on the blood pressure. In the present study we evaluated the nitric oxide contribution of the regulation of angiotensin II-induced vasoconstriction in normotensive rats and aortic coarctation-induced hypertensive rats. Renal vascular reactivity to angiotensin II was evaluated in the presence and absence of nitric oxide synthesis inhibitor; NG-nitro-L-arginine methyl ester. Nitrite concentration in perfusate was measured as an index of nitric oxide released and nitric oxide synthase activity was determined by production of 3H-L-citrulline. Renal NG-nitro-L-arginine methyl ester perfusion potentiated angiotensin II-induced vasoconstriction in normotensive rats but did not affect angiotensin II effect on hypertensive rats. The release of nitrites was lower in the kidneys from hypertensive rats than normotensive rats. Renal nitric oxide synthase activity was decreased in the hypertensive rats compared to the normotensive rats. We suggest that in normotensive rats, nitric oxide counteracts angiotensin II vasoconstrictor action, whereas, in hypertensive rats this mechanism is impaired, therefore, potentiating angiotensin II increase in vascular resistance thereby contributing to the developing of high blood pressure.