Renal vasoconstriction by vasopressin V1a receptors is modulated by nitric oxide, prostanoids, and superoxide but not the ADP ribosyl cyclase CD38.

Renal vasoconstriction by vasopressin V1a receptors is modulated by nitric oxide, prostanoids, and superoxide but not the ADP ribosyl cyclase CD38. Am J Physiol Renal Physiol. 2014 Mar 12; Authors: Moss NG, Kopple TE, Arendshorst WJ Abstract Renal blood flow (RBF) responses to arginine vasopressin (AVP) were tested in anesthetized wild-type (WT) and CD38(-/-) mice that lack the major calcium mobilizing second messenger cyclic ADP ribose. AVP (3-25 ng) injected iv produced dose-dependent decreases in RBF, reaching a maximum of 25±2% below basal RBF in WT and 27±2% in CD38(-/-) mice with 25 ng of AVP. Renal vascular resistance (RVR) increased 75±6% and 78±6% in WT and CD38(-/-) mice. Inhibition of NO synthase with L-NAME increased the maximum RVR response to AVP to 308±76% in WT and 388±81% in CD38(-/-) (P<0.001 for both). Cyclooxygenase inhibition with indomethacin increased the RVR response to 125±15% in WT and 120±14% in CD38(-/-) mice (P<0.001, <0.05). Superoxide suppression with tempol inhibited the RVR response to AVP by 38% in both strains (p<0.005), but was ineffective when administered after L-NAME. The rate of RBF recovery (relaxation) after AVP was slowed by L-NAME and indomethacin (P<0.001, <0.005), but was unchanged by tempol. Vascular responses to AVP were abolished by an AVP V1a receptor antagonist. A V2 receptor agonist or antagonist had no effect on AVP-induced renal vasoconstriction. The results indica...
Source: Am J Physiol Renal P... - Category: Urology & Nephrology Authors: Tags: Am J Physiol Renal Physiol Source Type: research