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 prostanoids with and without endothelium in basal conditions and in response to acetylcholine (ACh) stimulation was investigated. Isolated and perfused mesenteric vascular bed released 6-keto-prostaglandin F1 α and thromboxane B 2 (TXB 2) (stable metabolites of prostacyclin (PGI 2) and TXA 2, respectively), and also prostaglandin E 2 (PGE 2) and PGF 2α. PGI 2 was the major prostanoid formed by the mesenteric vascular bed. ACh 10 −5 M markedly increased PGI 2 release without any effect on the other prostanoids. Atropine 10 −6 M added to the perfusion medium previous to ACh reduced the release of PGI 2. Atropine alone did not modify the basal prostanoid pattern. Removal of endothelium with 96% ethanol produced a 50% reduction in the production of PGI 2 and TXA 2 with respect to basal values, without modifying PGE 2 or PGF 2α. Cholinergic stimulation by ACh of the de-endothelialized mesenteric vascular bed significantly increased only TXA 2 production. Atropine prevents this response to ACh. Our results indicate that in mesenteric vascular bed, endothelium mainly produces a potent vasodilator prostanoid, PGI 2, but also a lesser proportion of TXA 2. ACh, in stimulating muscarinic receptors, induces the production and release of PGI 2 from endothelium and TXA 2 from vascular smooth muscle when the endothelium is absent.