To study the effects of Ca-antagonistic drug, nifedipine, on receptor operated systemic and renal vascular reactivities to angiotensin II (A II), norepinephrine (NE), vasopressin (VP), bradykinin (BK) and prostaglandin E2 (PGE2), Japanese white rabbits weighing 3.2 to 3.9 kg (n=38) were used. Anesthesia was introduced by urethan (450 mg/kg) and a-chlorarose (45 mg/kg). Catheters were placed into the abdominal aorta (PE 60) through the femoral artery and into the vena cava inferior through the femorall vein (PE 50). For blood flow measurement, the lelt renal artery was exposed through a flank incision. A 27 gauge needle was inserted into the left renal artery for the infusion of vasoactive substances. Renal blood flow was measured by an electromagnetic flow meter. Systemic and renal vascular reactivities to All, NE, VP, BK and PGE2 were studied before and after the administration of nifedipine (50 μg/kg) intravenously. The intrarenal infusion of nifedipine (0.5, 1.0, and 2.5 μg/kg/min) produced a dose dependent increse in renal blood flow. pressor responses to vasopression (10, 20, and 50 mU /kg/min) and angiotensin II at low dose (10 ng/kg/min) was significantly diminished after the administration of nifedipine (50 μg/kg), whereas it had no effect at high doses of AII (20, 50 and 100 ng/kg/min) and norepinephrine (0.25, 0.5, 1.0 and 2.5 μg/kg/min). The decrease of renal blood flow induced by the intrarenal infusion of angiotensin II (2.5, 5.0 and 10 ng/kg/min) was attenuated significantly after the administration of nifedipine. The decrease of renal blood flow induced by the intrarenal infusion of vasopressin (10, 20 and 50 mU/kg/min) was also attenuated by nifedipine. However, the renel vasoconstrictor reaction to norepinephpine (25, 50 and 100ng/kg/ min) did not change significantly after the administration of nifedipine. The increased renal blood flow induced by the intrarenal infusion of bradykinin (2.5, 5.0 and 10ng/kg/ min) and prostaglandin E2 (20, 50 and 100 ng/kg/min) was not affected by nifedipine. These results suggest that receptor operated vasoconstrictor reaction to All and VP is mediated through the same Ca++ mobilization mechanism but that of NE is not. It is confirmed that the renal vasodilator effect of BK and PGE2 is not modulated bynifedipine in anesthetized rabbits.
