Abstract
Abstract Rat portal vein and mesentric arteries are frequently used as models for resistant vessels. In the present study the role of endothelium and cGMP in the reactivity of these vessels were studied. In one group of experiments, the endothelium was removed from both tissues by perfusion with distilled water. In another group, methylene blue (MBI, guanylate cyclase inhibitor)q\ was used to alter the GMP level. In all experiments, the vessel tone was elevated by noradrenaline NA before the addition of different vasodilators acetylcholine, Ach, ntroprusside, NP, verapamil, VP, and papaverine, PAPA. In mesenteric arteries, endothelium removal enhanced NA responses. The dilator response to NP, VP, or PAP were unaffected by endothelium removal or MBI. However, the relaxant effects of Ach were markedly inhibited by endothelium removal and MBI. In the portal vein endothelium removal and MBI were without effect on the responses to NA, VP or PAP, whereas, dilator responses to NP were markedly reduced by MBI but unaffected by endothelium removal. Ach caused only constriction in portal vein. These results show that venous endothelium play a less important role in the modulation of vascular reactivity than those the arterial endothelium. C GMP may play role in the relaxants effects of NP in the portal vein but not in mesenteric arteries. The present work support the hypothesis that Ach-induced relaxation is dependent on endothelium and c GMP.