Pressure-mediated vasoconstriction of juxtamedullary afferent arterioles involves p2 purinoceptor activation. Inscho, Edward W., Anthony K. Cook, and L. Gabriel Navar. Department of Physiology, Tulane University School of Medicine, New Orleans, LA 70112
APStracts 3:0148F, 1996.
This study was conducted to examine the hypothesis that P2 purinoceptors contribute to pressure-induced autoregulatory adjustments of afferent arteriolar caliber. Experiments were performed in-vitro using the blood-perfused juxtamedullary nephron technique. Afferent arteriolar diameter averaged 19.2 +/- 0.6_m (n=51) at control perfusion pressure of 100mmHg and decreased when perfusion pressure was increased. Desensitization of P2 purinoceptors abolished the [alpha],[beta]-methylene ATP-mediated afferent vasoconstriction and prevented pressure-dependent autoregulatory adjustments in afferent diameter. P2 purinoceptor saturation significantly decreased afferent caliber and attenuated pressure -induced autoregulatory responses. To block P2 receptors, afferent arterioles were treated with the P2 purinoceptor antagonists, PPADS or suramin. P2 receptor blockade, prevented the afferent arteriolar vasoconstriction evoked by increasing perfusion pressure from 100 to 130 and 160mmHg. These data demonstrate that inhibition of P2 purinoceptor-dependent responses through receptor desensitization, receptor saturation or purinoceptor blockade impair normal autoregulatory behavior in rat juxtamedullary afferent arterioles. The results are consistent with the hypothesis that P2 purinoceptors participate in mediating autoregulatory adjustments in afferent arteriolar diameter. 

Received 20 March 1996; accepted in final form 15 August 1996.
APS Manuscript Number F94-6.
Article publication pending Am. J. Physiol. (Renal Fluid Electrolyte
Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 29 August 1996