Paradoxical Vasoconstriction Induced by Acetylcholine in Atherosclerotic Coronary Arteries
- 23 October 1986
- journal article
- research article
- Published by Massachusetts Medical Society in New England Journal of Medicine
- Vol. 315 (17), 1046-1051
- https://doi.org/10.1056/nejm198610233151702
Abstract
Acetylcholine is believed to dilate normal blood vessels by promoting the release of a vasorelaxant substance from the endothelium (endothelium-derived relaxing factor). By contrast, if the endothelium is removed experimentally, acetylcholine constricts blood vessels. We tested the hypothesis that muscarinic cholinergic vasodilation is impaired in coronary atherosclerosis.This publication has 24 references indexed in Scilit:
- Short- and long-term interactions of endothelium and vascular smooth muscle in coculture: effects on cyclic GMP production.Proceedings of the National Academy of Sciences, 1986
- New insights into the cellular mechanisms of vasospasThe American Journal of Cardiology, 1985
- Endothelium-derived vascular relaxing factor.Hypertension, 1985
- A double-blind, placebo-controlled study of ketanserin in patients with Prinzmetal's angina. Evidence against a role for serotonin in the genesis of coronary vasospasm.Circulation, 1984
- alpha-Adrenergic receptors and coronary spasm: an elusive link.Circulation, 1984
- Role of endothelium in responses of vascular smooth muscle.Circulation Research, 1983
- Sudden death in prinzmetal's angina with coronary spasm documented by angiography: Analysis of three necropsy patientsThe American Journal of Cardiology, 1982
- Effects of intravenous prostacyclin in variant angina.Circulation, 1982
- Thromboxane A2in Vasotonic Angina PectorisNew England Journal of Medicine, 1981
- The obligatory role of endothelial cells in the relaxation of arterial smooth muscle by acetylcholineNature, 1980