Related Experiment Video
Updated: Aug 10, 2026

Quantifying Agonist Activity at G Protein-coupled Receptors
Published on: December 26, 2011
Evidence that PGE2 stimulates intestinal epithelial cell adenylate cyclase by a receptor-mediated mechanism
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, gamma S-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.
Related Concept Videos
Amplifying Signals via Second Messengers
GPCRs Regulate Adenylyl Cylase Activity
Two...
cAMP-dependent Protein Kinase Pathways
Pathophysiology of Peptic Ulcer Disease: Injurious Factors
In the antrum region, G cells secrete the gastrin hormone that binds to gastrin-cholecystokinin-B (CCK2) receptors on parietal and enterochromaffin-like (ECL) cells in the fundic glands. Simultaneously, the vagus nerve releases acetylcholine, which binds to M3...
Drugs for Peptic Ulcer Disease: Prostaglandin Analogs as Mucosal Protective Agents
Non-steroidal anti-inflammatory drugs (NSAIDs) can induce peptic ulcers by inhibiting cyclooxygenase, decreasing...
Gastritis II: Pathophysiology

