EFFECTS OF NIFEDIPINE AND TMB-8 ON ANGIOTENSIN-II-INDUCED ANTINATRIURESIS IN ANESTHETIZED DOGS

A calcium entry blocker, nifedipine, or an intracellular calcium relea se inhibitor, TMB-8, was infused into the renal artery before and duri ng intravenous infusion of angiotensin II in anesthetized dogs. In the control period, nifedipine (0.1 mu g/kg/min) or TMB-8 (75 mu g/kg/min ) increased urine flow rate, urinary sodium excretion and fractional s odium excretion, with little change: in renal blood flow or glomerular filtration rate. Angiotensin II (10 ng/kg/min) elevated blood pressur e and reduced urine flow rate, urinary sodium excretion and fractional sodium excretion. In the angiotensin II infusion period, nifedipine i ncreased urine flow rate, urinary sodium excretion and fractional sodi um excretion to levels higher than those observed in the control perio d. TMB-8 also caused augmented urinary responses. The results suggest that the angiotensin II-induced antinatriuresis depends both on the ca lcium influx through dihydropyridine-sensitive calcium channels, and o n the calcium release from TMB-8-sensitive calcium stores at the renal tubular sites.