Stability of the vasopressin V2 receptor-adenylyl cyclase system in rat kidney.
In the Brattleboro rat with diabetes insipidus vasopressin V2 receptor mRNA and the mRNA of various adenylyl cyclase (AC) isoforms are moderately reduced compared with those of normal rats. In the present study renal vasopressin V2 receptor mRNA was modestly higher (by 34%), as was expression of AC 5, 6 and 9 mRNAs (up to 22% greater), in BDI rats treated with the vasopressin V2 receptor agonist desamino-[Arg8] vasopressin than in untreated controls. AC 4 mRNA was decreased by 17% following desamino-[Arg8s] vasopressin treatment. While the stimulatory Gsalpha mRNA was little affected by the desamino-[Arg8] vasopressin treatment, two of the inhibitory G proteins were raised (Galphai-2 by 54% and Galphai-3 by 57%). Treatment of Sprague-Dawley rats with a specific vasopressin V2 receptor antagonist (SR 121463A) was not associated with any marked changes in mRNA expression. These results indicate that the vasopressin V2 receptor adenylyl cyclase system mediating the antidiuretic response to vasopressin is relatively stable. The Gi proteins may be involved in the stabilizing mechanism.