Effects of nifedipine and TMB-8 on angiotensin II-induced antinatriuresis in anesthetized dogs

A. Takahara, H. Hisa, M. Yoshida, M. Suzuki-Kusaba, S. Satoh

Research output: Contribution to journalArticle

1 Citation (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)309-318
Number of pages10
JournalArchives Internationales de Pharmacodynamie et de Therapie
Volume330
Issue number3
Publication statusPublished - 1995 Dec 1

ASJC Scopus subject areas

  • Pharmacology

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