Renal excretion of prostaglandins E2 and F2alpha in diabetes insipidus rats.

Abstract

On the assumption that the antagonism between prostaglandin E2 and vasopressin might represent a negative feedback system, we evaluated the hypothesis that vasopressin stimulates, in vivo, the renal production of prostaglandins. For these studies we used Brattleboro homozygous rats with diabetes insipidus and Long-Evans rats for controls, Brattleboro homozygotes show a substantial reduction in the renal excretion of prostaglandin E2 and prostaglandin F2alpha. Homozygotes excreted 39 +/- 5 ng/24 h prostaglandin E2 and 40 +/- 4 ng/24 h prostaglandin F2alpha, compared to 217 +/- 40 and 221 +/- 18 ng/24 h, respectively, in control rats (P less than 0.001). Therapy of homozygotes with vasopressin tannate in oil resulted in a prompt increase in the urinary excretion of prostaglandin E2 and prostaglandin F2alpha. 1-Desamino-D-arginine vasopressin, a nonpressor analogue of vasopressin, also enhanced the renal production of prostaglandin E2. We conclude that vasopressin (antidiuretic hormone) stimulates renal production and excretion of prostaglandin E2 and prostaglandin F2alpha in vivo. It is possible that this increment of prostaglandin synthesis serves a negative feedback function by modulating the action of vasopressin on the renal tubule.