When the inhibitory prostanoid EP receptor is stimulated, production of the second messenger cAMP is decreased via inhibition of the adenylate cyclase enzyme. This leads to a decrease in cytosolic concentrations of cAMP and the ability of protein kinase A to phosphorylate H+/K+ATPase (proton pump).

In parietal cells, prostaglandins inhibit the adenylate cyclase-initiated activity that is stimulated by histamine. This is in contrast to most other tissues, where prostaglandins stimulate adenylate cyclase activity and increase intracellular formation of cAMP, resulting in fluid secretion.

Misoprostol is a synthetic prostaglandin E1 analogue, which reduces acid secretion in a dose-dependent manner. It also has mucosal protective properties. Therefore, misoprostol is used as an adjunct to reduce the incidence of NSAID-induced ulceration. However, the cost-effectiveness of this co-therapy remains controversial. Furthermore, compliance can be a problem due to the dose-dependent diarrhoea that results from its administration.

For an overview of prostaglandin synthesis click here.


Misoprostol promotes ulcer healing through: