NITRIC-OXIDE MAY PARTICIPATE IN V-2 VASOPRESSIN-RECEPTOR-MEDIATED RENAL VASODILATION

Using pentobarbital-anesthetized euvolemic dogs, we investigated whether vasopressin V-2-receptor stimulation induced renal vasodilation and whether nitric oxide (NO) had a role in the process. Intrarenal infusion of arginine-vasopressin (AVP) resulted in renal vasoconstriction with presser response. After preadministration of a V-2-receptor antagonist, however, intrarenal infusion of AVP caused an increase in renal blood flow (RBF) without presser action, indicating renal vasodilation. This renal vasodilation was not observed when we infused AVP after-simultaneous pretreatment with V-1- and V-2-receptor antagonists. Even in the absence of the V-2-receptor antagonist, this renal vasodilation was attenuated by intrarenal infusion of L-N-G-nitroarginine (L-NNA). Concomitant infusion of L-arginine prevented the inhibitory effect of L-NNA on renal vasodilation induced by intrarenal infusion of AVP in the presence of the V-1-antagonist. These data indicate that the renal vasodilation caused by intrarenal infusion of AVP in the presence of a V-1-antagonist was mediated by V-2-receptor stimulation, and the inhibitory effect of L-NNA on V-2-receptor-mediated renal vasodilation was attributed to its inhibitory effect on NO synthesis, suggesting that NO may participate in V-2-receptor-mediated renal vasodilation.