Increased vascular responsiveness to bradykinin in kidneys of spontaneously hypertensive rats. Effect of N omega-nitro-L-arginine.

摘要: We investigated the role of nitric oxide (NO)-dependent and NO-independent mechanisms in mediation renal vasodilatory responses to bradykinin spontaneously hypertensive rats (SHR), with angiotensin II-induced hypertension (200 ng/min i.p. for 6 days) corresponding normotensive control Wistar-Kyoto (WKY) sham-infused rats. To this end, we contrasted effects arterial injections other vasodilators, acetylcholine sodium nitroprusside, on perfusion pressure output cyclic GMP isolated kidneys perfused Krebs bicarbonate buffer containing phenylephrine, both without N omega-nitro-L-arginine (L-NOARG) (50 microM), an inhibitor NO synthetase. In L-NOARG, all agonists increased reduced pressure, indicative vasodilation. were attenuated, associated abolished, suggesting dependency synthesis. Irrespective whether or SHR more responsive than WKY regard bradykinin-induced contrast, responsiveness was nearly equal controls. Also, nitroprusside similar These data suggest that vasculature is uniquely selectively hyperresponsive bradykinin, NO-dependent actions.