DIFFERENT RESPONSES OF RENAL BLOOD-FLOW AND SYMPATHETIC-NERVE ACTIVITY TO CAPTOPRIL AND NICARDIPINE IN CONSCIOUS RENAL HYPERTENSIVE RABBITS

To elucidate the roles of endogenous angiotensin II (AII) and renal sympathetic nerve activity (RSNA) in modulation of renal blood flow (RBF), we recorded RBF and RSNA in conscious two-kidney, one-clip (2K1C) hypertensive rabbits with blood pressure (BP) reduced to a similar extent by captopril (5 mg/kg) and nicardipine (4.3 mu g/kg/min). We measured plasma concentrations of AII, arginine vasopressin (AVP), and norepinephrine (NE). Despite comparable depressor effects, changes in RBF showed different profiles with the two drugs in renal hypertensive rabbits. After captopril injection, RBF was consistently increased to 143 +/- 7%. In contrast, with nicardipine infusion, RBF was initially increased to 114 +/- 5% and then significantly decreased to 86 +/- 4%. The increase in RSNA was greater with captopril than with nicardipine. Plasma concentration of AII was decreased with captopril but significantly increased with nicardipine. In sham-clipped normotensive rabbits in which plasma AII was not increased, RBF was not reduced with nicardipine. Thus, vasoconstrictor actions of RSNA and increased AII may have overcome the vasodilatory effect of nicardipine in conscious renal hypertensive rabbits. Because the increase in RSNA was smaller with nicardipine, we speculate that the vasoconstriction induced by AII, as well as background BP level, played a substantial role in determining RBF.