STABILITY OF THE VASOPRESSIN V-2 RECEPTOR-ADENYLYL CYCLASE SYSTEM IN RAT-KIDNEY

In the Brattleboro rat with diabetes insipidus vasopressin V-2 recepto r mRNA and the mRNA of various adenylyl cyclase (AC) isoforms are mode rately reduced compared with those of normal rats. In the present stud y renal vasopressin V-2 receptor mRNA was modestly higher (by 34%), as was expression of AC 5, 6 and 9 mRNAs (up to 22% greater), in BDI rat s treated with the vasopressin V-2 receptor agonist desamino-[Arg(8)] vasopressin than in untreated control. AC 4 mRNA was decreased by 17% following desamino-[Arg(8)] vasopressin treatment. While the stimulato ry Gs cy mRNA was little affected by the desamino-[Arg8(]) vasopressin treatment, two of the inhibitory G proteins were raised (G alpha i-2 by 54% and G alpha i-3 by 57%). Treatment of Sprague-Dawley rats with a specific vasopressin V-2 receptor antagonist (SR 121463A) was not as sociated with any marked changes in mRNA expression. These results ind icate that the vasopressin V-2 receptor adenylyl cyclase system mediat ing the antidiuretic response to vasopressin is relatively stable. The Gi proteins may be involved in the stabilizing mechanism, (C) 1998 El sevier Science B.V.