CONTROL OF RENAL MEDULLARY BLOOD-FLOW BY VASOPRESSIN V-1 AND V-2 RECEPTORS

Experiments were performed in anesthetized renal-denervated rats to de termine the contribution of renal medullary vasopressin V-1 and V-2 re ceptor stimulation in the regulation of renal medullary blood flow. Re nal medullary interstitial infusion of the selective V-1 agonist [Phe( 2), Ile(8), Orn(8)] vasopressin (2 ng . kg(-1). min(-1)) significantly decreased outer medullary blood flow by 15% and inner medullary blood flow by 35%, as measured with implanted optical fibers for laser-Dopp ler flowmetry. Medullary interstitial infusion of equimolar doses of a rginine vasopressin (AVP) also decreased outer medullary blood flow by 15% but decreased inner medullary blood flow by only 17%, a decrease significantly less than that during the infusion of the V-1 agonist. T hese results were confirmed in videomicroscopy experiments on the expo sed papilla, which demonstrated that the V-1 agonist and AVP decreased descending and ascending vasa recta capillary red blood cell velocity and calculated blood flow, with greater decreases during infusion of the V-1 agonist. In further laser-Doppler flowmetry studies, stimulati on of V-2 receptors by medullary interstitial infusion of 1-desamino-8 -D-arginine vasopressin (2 ng . kg(-1). min(-1)) or AVP in rats pretre ated with the vasopressin V-1 receptor antagonist d(CH2)(5)[Tyr(Me)(2) , Ala-NH2]AVP increased renal medullary blood flow by 16 +/- 3 and 27 +/- 8%, respectively. The present experiments indicate that vasopressi n V-1 receptor stimulation serves to decrease renal medullary blood fl ow while V-2 receptor stimulation appears to increase renal medullary blood flow; however, the net effect of AVP is to decrease renal medull ary blood flow.