A calcium entry blocker, nifedipine, or an intracellular calcium release inhibitor. TMB-8, was infused into the renal artery before and during intravenous infusion of angiotensin II in anesthetized dogs. In the control period, nifedipine (0.1 μg/kg/min) or TMB-8 (75 μg/kg/min) increased urine flow rate, urinary sodium excretion and fractional sodium excretion, with little change in renal blood flow or glomerular filtration rate. Angiotensin II (10 ng/kg/min) elevated blood pressure and reduced urine flow rate, urinary sodium excretion and fractional sodium excretion. In the angiotensin II infusion period, nifedipine increased urine flow rate, urinary sodium excretion and fractional sodium excretion to levels higher than those observed in the control period. TMB-8 also caused augmented urinary responses. The results suggest that the angiotensin II-induced antinatriuresis depends both on the calcium influx through dihydropyridine- sensitive calcium channels, and on the calcium release from TMB-8-sensitive calcium stores at the renal tubular sites.
|ジャーナル||Archives Internationales de Pharmacodynamie et de Therapie|
|出版ステータス||Published - 1995|
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