Inhibition of ADH-enhanced transepithelial urea and water movement by prostaglandins.

The effects of PGF2 alpha and PGE2 on transepithelial urea flux and osmotic water flow were evaluated in total bladders. Mucosal to serosal urea flux and osmotic water flow were not changed from basal values by the addition of either prostaglandin to the serosal bath. However, treatment with either PGF2 inhibited both urea flux and osmotic water flow in response to ADH stimulation in a concentration-dependent manner. The hydrosmotic response to ADH was more sensitive to prostaglandin inhibition than was urea flux. The inhibitory effect of the prostaglandins on ADH-enhanced urea flux was not dependent upon inhibition of the hydrosmotic response, since both PGF2 alpha and PGE2 decreased urea flux in the absence of a transepithelial osmotic gradient. Prostaglandin E2 was a more potent inhibitor than PGF2 alpha of both ADH-enhanced urea flux and osmotic water flow. The PGF2 alpha antagonism of osmotic water flow was apparently competitive, while antagonism of urea flux was apparently noncompetitive. The results are consistent with the hypothesis of the existence of a "spare" population of prostaglandin receptors that modulate water flow, but the absence of a "spare" prostaglandin receptor population with respect to the modulation of urea flux.