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Alpha-1 adrenoceptor subtypes involved in mediating adrenergically induced antinatriuresis and antidiuresis in two kidney, one clip Goldblatt and deoxycorticosterone acetate-salt hypertensive rats

MA Sattar and EJ Johns

Department of Physiology, The Medical School, Birmingham, United Kingdom.

This study characterized the alpha-1 adrenoceptor subtypes involved in adrenergically induced antinatriuresis and antidiuresis in pentobarbital-anesthetized deoxycorticosterone acetate (DOCA)-salt and two kidney, one clip (2K1C) Goldblatt hypertensive rats. In the DOCA- salt rats, phenylephrine infusion (100 microgram kg(-1) hr(-1) close renal arterially) caused increases in blood pressure of 5 to 10%, decreases in renal blood flow of 5 to 12%, whereas there were large reversible decreases in urine flow and absolute and fractional sodium excretions of 55 to 70%. The presence of chloroethylclonidine (10 microgram kg(-1) hr(-1) to block alpha-1B adrenoceptors) had no effect on the magnitude of the phenylephrine-induced excretory responses, but after 5-methylurapidil (10 microgram kg(-1) hr(-1) to block alpha-1A adrenoceptors) they were abolished. Infusion of phenylephrine in the 2K1C hypertensive rats caused small hemodynamic and renal blood flow responses with marked 55 to 70% reductions in urine flow and absolute and sodium excretion. The phenylephrine-induced antinatriuresis and antidiuresis, which was probably due to activation of alpha-1 adrenoceptors present on the renal tubular epithelial cells, and the fact that these tubular responses were blocked by 5-methylurapidil but not by chloroethylclonidine in both DOCA-salt and 2K1C Goldblatt hypertensive models, means that the alpha-1A adrenoceptors was the major functional subtype present.

Volume 277, Issue 1, pp. 245-252, 04/01/1996
Copyright © 1996 by American Society for Pharmacology and Experimental Therapeutics




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Copyright © 1996 by the American Society for Pharmacology and Experimental Therapeutics.