Effect of PGE1, indomethacin, and polyphloretin phosphate on toad bladder response to ADH.

ALBERT, ~VILLIAM C., AND JOSEPH S. HANDLER. EJect of PGEl, indomethacin, and fo&hloretin phosphate on toad bladder response to ADH Am. J. Physiol, 226(6) : 1382-l 386. 1974.-Exogenous PGEr inhibits the short-circuit current response, as well as the water permeability response of the toad bladder to vasopressin. Since PGEI does not inhibit either response to cyclic AMP, it is thought to act by inhibiting the effect of vasopressin on adenylate cyclase. Indomethacin, an inhibitor of prostaglandin synthesis, and polyphloretin phosphate, a prostaglandin antagonist, were used in an attempt to evaluate the rcle of enclogenous prostaglandins in the water permeability response to vasopressin. Both agents enhanced the response to vasopressin and to cyclic AMP. Although the enhancement may be related to decreased activity of endogenous prostaglandins and/or to inhibition of cyclic AMP breakdown by cyclic nucleotide phosphodiesterase, neither mechanism explains the effects of these agents in the presence of exogenous PGEl. Under these conditions, indomethacin had no effect on the response to vasopressin, but still enhanced the response to cyclic AMP; polyphloretin phosphate inhibited the response to vasoprecsin and had no effect on the response to cyclic AMP.