PT  - JOURNAL ARTICLE
AU  - A M Elhawary
AU  - W A Pettinger
AU  - D W Wolff
TI  - Subtype-selective alpha-1 adrenoceptor alkylation in the rat kidney and its effect on the vascular pressor response.
DP  - 1992 Feb 01
TA  - Journal of Pharmacology and Experimental Therapeutics
PG  - 709--713
VI  - 260
IP  - 2
4099  - http://jpet.aspetjournals.org/content/260/2/709.short
4100  - http://jpet.aspetjournals.org/content/260/2/709.full
SO  - J Pharmacol Exp Ther1992 Feb 01; 260
AB  - Separate genes for alpha-1A and alpha-1B adrenoceptors have now been identified. Whereas alpha-1 adrenoceptors are known to mediate rat renal vasoconstriction, the relative importance of these alpha-1 adrenoceptor subtypes was unknown. We cannulated the right suprarenal artery of anesthetized male Sprague-Dawley rats to permit administration of the alpha-1A and alpha-1B alkylating antagonists, SZL-49 (SZL) and chloroethylclonidine (CEC), respectively, directly into the right kidney. Treated kidneys were homogenized to identify the doses of SZL and CEC that caused the maximum reductions in Bmax for [3H]prazosin, the relatively nonselective alpha-1 adrenoceptor antagonist. In other rats, a Doppler flow probe was placed around the right renal artery, and dose-peak response curves for boluses of the alpha-1 adrenoceptor agonist phenylephrine (PHE) were generated before and after supramaximal dosages of SZL or CEC. Renal vasoconstriction to PHE was nearly obliterated by SZL. In contrast, CEC caused only a modest rightward shift in the PHE DRC. SZL also abolished the renal vascular response to two other alpha-1 adrenoceptor agonists, cirazoline and methoxamine. Our data support the conclusion that the alpha-1 adrenoceptors at the level of the rat renal resistance vessels are predominantly alpha-1A adrenoceptors.