Abstract
The effects of PGF 2α and PGE 2 on transepithelial urea flux and osmotic water flow were evaluated in toad 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 PGF 2α or PGE 2 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 PGF 2α and PGE 2 decreased urea flux in the absence of a trans-epithelial osmotic gradient. Prostaglandin E 2 was a more potent inhibitor than PGE 2α of both ADH-enhanced urea flux and osmotic water flow. The PGF 2α antagonism of osmotic water flow was apparently competitive, while antagonism of urea flux was apparently non-competitive. 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.
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