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An intracellular calcium release inhibitor TMB-8 suppresses renal nerve stimulation-induced antinatriuresis in dogs

A Ogasawara, H Hisa and S Satoh

Department of Pharmacology, Tohoku University, Sendai, Japan.

Effects of nifedipine and TMB-8 on antinatriuresis induced by renal nerve stimulation (RNS) were examined in pentobarbital-anesthetized dogs. RNS (1 Hz) decreased urine flow rate, urinary sodium excretion rate and fractional excretion of sodium and increased renal norepinephrine efflux and renal venous plasma renin activity with little changes in renal hemodynamics. Intrarenal arterial infusion of nifedipine (0.1 microgram/kg/min) or TMB-8 (50 and 100 micrograms/kg/min) increased basal urine flow rate, urinary sodium excretion rate and fractional excretion of sodium without affecting renal venous plasma norepinephrine concentration or plasma renin activity. Neither nifedipine nor TMB-8 affected the RNS-induced increases in norepinephrine efflux and plasmin renin activity. The RNS- induced decreases in urinary sodium excretion rate and fractional excretion of sodium were suppressed during the TMB-8 infusion, whereas nifedipine failed to affect these urinary responses. These results raise the possibility that the release of intracellular calcium from TMB-8-sensitive stores, but not the influx of extracellular calcium through dihydropyridine-sensitive calcium channels, participates in neural control of tubular sodium reabsorption in the dog kidney.

Volume 264, Issue 1, pp. 117-121, 01/01/1993
Copyright © 1993 by American Society for Pharmacology and Experimental Therapeutics




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Copyright © 1993 by the American Society for Pharmacology and Experimental Therapeutics.