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Pharmacodynamics:
Cytotec has both antisecretory (inhibiting gastric acid secretion) and (in
animals) mucosal protective properties. NSAIDs inhibit prostaglandin synthesis, and a deficiency of
prostaglandins within the gastric mucosa may lead to diminishing bicarbonate and mucus secretion and
may contribute to the mucosal damage caused by these agents. Misoprostol can increase bicarbonate
and mucus production, but in man this has been shown at doses 200 mcg and above that are also
antisecretory. It is therefore not possible to tell whether the ability of misoprostol to reduce the risk of
gastric ulcer is the result of its antisecretory effect, its mucosal protective effect, or both.
In vitro studies on canine parietal cells using tritiated misoprostol acid as the ligand have led to the
identification and characterization of specific prostaglandin receptors. Receptor binding is saturable,
reversible, and stereospecific. The sites have a high affinity for misoprostol, for its acid metabolite, and
for other E type prostaglandins, but not for F or I prostaglandins and other unrelated compounds, such
as histamine or cimetidine. Receptor-site affinity for misoprostol correlates well with an indirect index of
antisecretory activity. It is likely that these specific receptors allow misoprostol taken with food to be
effective topically, despite the lower serum concentrations attained.
Misoprostol produces a moderate decrease in pepsin concentration during basal conditions, but not
during histamine stimulation. It has no significant effect on fasting or postprandial gastrin nor on intrinsic
factor output.
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Topic revision: r2 - 17 Aug 2008 - 17:28:57 -
CytoTec