Modulation by prostaglandins of the renal vascular action of arginine vasopressin.

To determine whether the renal vascular effect of arginine vasopressin (AVP) is modulated by renal prostaglandins, renal blood flow (RBF) and renal venous plasma prostaglandin E2 (PGE2) were determined during the infusion of AVP in dogs during control conditions and after the administration of the inhibitor of prostaglandin synthesis, indomethacin. During control conditions, intrarenal administration for 10 min of a dose of AVP calculated to increase arterial renal plasma AVP concentration by 75 pg/ml produced a slight renal vasodilation (p less than 0.01) and an increase in renal venous plasma concentration of PGE2. Renal venous PGE2 concentration during control and AVP infusion averaged 33 +/- 7(2) and 52 +/- 12 pg/ml (p less than 0.05), respectively. After administration of indomethacin, the same dose of AVP induced renal vasoconstriction (p less than 0.05) and failed to enhance renal venous PGE2 concentration (9 +/- 1 to 8 +/- 1 pg/ml). Intrarenal administration of 20 ng/kg . min of AVP for 10 min induced a marked renal vasoconstriction (p less than 0.01) and increased renal venous plasma PGE2. Renal venous PGE2 during control and AVP infusion averaged 31 +/- 10 and 121 +/- 31 pg/ml (p less than 0.01), respectively. Administration of the same dose of AVP following indomethacin produced a significantly greater and longer lasting renal vasconstriction (p less than 0.01) and failed to increase renal venous plasma PGE2 (10 +/- 1 to 9 +/- 1 pg/ml). These results indicate that a concentration of AVP comparable to that observed in several pathophysiological conditions induces a slight renal vasodilation which is mediated by renal prostaglandins. The results also indicate that higher doses of AVP induce renal vasoconstriction and that prostaglandin synthesis induced by AVP attenuates the renal vasoconstriction produced by this peptide.