| Literature DB >> 1715111 |
Abstract
An altered release of endothelium-derived vasoactive factors has been implicated in several vasospastic conditions. Since the functional role of the endothelium in the hand vasculature is largely unknown, we examined the effects of 'endothelial removal' on vascular reactivity, and the effects of some 'endothelium-associated' substances in isolated human hand veins and arteries. Acetylcholine induced a large relaxation (Emax = 97 +/- 1%) in precontracted hand arteries. The relaxation was abolished by endothelial removal. In hand veins, acetylcholine induced a small relaxation (Emax = 13 +/- 4%), which was unaffected by endothelial removal. An endothelium-dependent relaxation was, however, obtained with high concentrations (greater than or equal to 10(-6) mol l-1) of the Ca2+ ionophore A23187. Contractile responses to noradrenaline, serotonin and prostaglandin F2 alpha did not differ between vein segments with and without endothelium. Endothelin was a potent constrictor of both veins and arteries. The potency and maximum response did not differ between the two types of vessel. Indomethacin pretreatment of veins did not influence the endothelin-induced contractions, suggesting that cyclo-oxygenase products are not involved in the response. In endothelin-contracted veins and arteries, the prostacyclin analogue iloprost elicited relaxation of similar potency and amplitude. The maximum relaxation in veins was, however, 3 times larger than that produced by prostacyclin itself. Platelet-activating factor was devoid of contractile and relaxant effects in both veins and arteries. The present study indicates differences between human hand veins and arteries regarding endothelial-dependent relaxation, and suggests that the modulatory role of endothelium-derived relaxing factor(s) is small in hand veins. The contractile and relaxant effects of endothelin and iloprost, however, did not differ between veins and arteries.Entities:
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Year: 1991 PMID: 1715111 DOI: 10.1111/j.1748-1716.1991.tb09144.x
Source DB: PubMed Journal: Acta Physiol Scand ISSN: 0001-6772