Evidence that PGE2 stimulates intestinal epithelial cell adenylate cyclase by a receptor-mediated mechanism

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Abstract
These studies were performed to examine whether prostaglandin E2 stimulates intestinal epithelial secretion via a receptor-mediated or non-receptor-mediated activation of adenylate cyclase. Solubilization of epithelial cell adenylate cyclase with Lubrol PX, which separates the receptor moiety of the cyclase from the remainder of the complex, inhibited the prostaglandin E2 stimulation of the cyclase. A similar result was obtained with VIP, which activates adenylate cyclase via a receptor-mediated mechanism, whereas fluoride, γS-GTP, and forskolin, which activate the cyclase via non-receptor-mediated mechanisms, all stimulated solubilized adenylate cyclase. In addition, prostaglandin E2 and VIP both showed a dependence on GTP for adenylate cyclase stimulation while fluoride and forskolin did not. These data suggest that prostaglandin E2 activates intestinal mucosal adenylate cyclase by a receptor-mediated mechanism. The presence of such receptors lends support to the possibility that prostaglandins have a physiological role in the control of mucosal transport.