Control of renal medullary blood flow by vasopressin V₁ and V₂ receptors

Experiments were performed in anesthetized renal-denervated rats to determine the contribution of renal medullary vasopressin V₁ and V₂ receptor stimulation in the regulation of renal medullary blood flow. Renal medullary interstitial infusion of the selective V₁ agonist [Phe²,Ile³,Orn⁸]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-Doppler flowmetry. Medullary interstitial infusion of equimolar doses of arginine 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 V₁ agonist. These results were confirmed in videomicroscopy experiments on the exposed papilla, which demonstrated that the V₁ 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 V₁ agonist. In further laser-Doppler flowmetry studies, stimulation of V₂ receptors by medullary interstitial infusion of 1-desamino-8-D-arginine vasopressin (2 ng · kg^-1 · min^-1) or AVP in rats pretreated with the vasopressin V₁ 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 vasopressin V₁ receptor stimulation serves to decrease renal medullary blood flow while V₂ receptor stimulation appears to increase renal medullary blood flow; however, the net effect of AVP is to decrease renal medullary blood flow.