EFFECT OF ENDOTHELIUM REMOVAL ON BASAL AND MUSCARINIC CHOLINERGIC STIMULATED RAT MESENTERIC VASCULAR BED PROSTANOID SYNTHESIS

The ability of the rat mesenteric vascular bed to synthesize prostanoi ds with and without endothelium in basal conditions and in response to acetylcholine (ACh) stimulation was investigated. Isolated and perfus ed mesenteric vascular bed released 6-keto-prostaglandin F1alpha and t hromboxane B2 (TXB2) (stable metabolites of prostacyclin (PGI2) and TX A2, respectively), and also prostaglandin E2 (PGE2) and PGF2alpha. PGI 2 was the major prostanoid formed by the mesenteric vascular bed. ACh 10(-5) M markedly increased PGI2 release without any effect on the oth er prostanoids. Atropine 10(-6) M added to the perfusion medium previo us to ACh reduced the release of PGI2. Atropine alone did not modify t he basal prostanoid pattern. Removal of endothelium with 96% ethanol p roduced a 50% reduction in the production of PGI2 and TXA2 with respec t to basal values, without modifying PGE2 or PGF2alpha. Cholinergic st imulation by ACh of the de-endothelialized mesenteric vascular bed sig nificantly increased only TXA2 production. Atropine prevents this resp onse to ACh. Our results indicate that in mesenteric vascular bed, end othelium mainly produces a potent vasodilator prostanoid, PGI2, but al so a lesser proportion of TXA2. ACh, in stimulating muscarinic recepto rs, induces the production and release of PGI2 from endothelium and TX A2 from vascular smooth muscle when the endothelium is absent.