Abstract
The purpose of our study was to examine the role of prostaglandins in angiotensin II (ANG II)-induced gastric vasoconstriction. ANG II produced statistically significant, dose-related increases in vascular resistance of a mechanically perfused ex vivo stomach segment of chloralose-anesthetized dogs. We next examined the effect of cyclooxygenase inhibitors on responses to ANG II. Indomethacin (10 mg/kg), which blocked the vasodilator response to intra-arterial arachidonic acid, augmented the maximal increase in perfusion pressure during ANG II infusion. Similar results were found using a different cyclooxygenase inhibitor, meclofenamic acid. In the final experiments we used an enzyme immunoassay to measure 6-ketoprostaglandin F1 alpha (6-keto-PGF1 alpha) plasma concentrations. ANG II produced dose-related increases in gastric venous but not arterial levels of 6-keto-PGF1 alpha, the major metabolite of prostacyclin. Our results are consistent with the hypothesis that release of vasodilatory prostaglandins attenuates the vasoconstrictor response to ANG II in the gastric microcirculation.
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