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Article: Spasm of the coronary arteries: Causes and consequences (the scientist's viewpoint)

TitleSpasm of the coronary arteries: Causes and consequences (the scientist's viewpoint)
Authors
Issue Date1985
PublisherDowden Health Media, Inc. The Journal's web site is located at http://www.mayoclinicproceedings.com
Citation
Mayo Clinic Proceedings, 1985, v. 60 n. 1, p. 33-46 How to Cite?
AbstractBoth β1- and α1-adrenoceptors are present on canine coronary arteries, and they are accessible to norepinephrine released from the sympathetic nerves. Under normal conditions, these arteries relax because of the predominance of the β1-adrenoceptors, whereas constriction prevails in the presence of β1-adrenoceptor antagonists. The coronary arteries also have cholinergic nerves. When activated, these nerves release acetylcholine, which acts on muscarinic receptors on the sympathetic nerve terminals to reduce the output of norepinephrine and thereby lessen the relaxation mediated by β1-adrenoceptors. Thus, muscarinic agonists can precipitate coronary artery spasm. If the smooth muscle cells of the coronary arteries become hypoxic, their responsivneness to β-adrenergic stimulation is lost and constrictor responses are exaggerated. Cardiac glycosides prevent the predominance of the β-adrenergic effects of norepinephrine. Therefore, after treatment with ouabain, release of norepinephrine from the sympathetic nerves leads not to relaxation but to further contraction of coronary arteries. The endothelium of the coronary arteries inhibits platelet aggregation by the formation and release of prostacyclin, and it reacts to platelet products by causing relaxation of the underlying smooth muscle. In addition, if any thrombin is formed, it also causes endothelium-mediated relaxation. If the endothelium is damaged, these protective mechanisms are lost. Patients with coronary artery spasm usually have morphologic changes in the artery at the site of the spasm. Platelets can aggregate at this site and release vasoactive substances, which - aided by formation of thrombin - cause contraction. Thus, the blood supply to the myocardium is reduced; the ensuing hypoxia augments the constriction. Acute myocardial ischemia caused by coronary vasospasm may precipitate acute cardiac rhythm disturbances and sudden death by ventricular tachycardia or fibrillation.
Persistent Identifierhttp://hdl.handle.net/10722/170783
ISSN
2015 Impact Factor: 5.92
2015 SCImago Journal Rankings: 2.456
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorShepherd, JTen_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:10:49Z-
dc.date.available2012-10-30T06:10:49Z-
dc.date.issued1985en_US
dc.identifier.citationMayo Clinic Proceedings, 1985, v. 60 n. 1, p. 33-46en_US
dc.identifier.issn0025-6196en_US
dc.identifier.urihttp://hdl.handle.net/10722/170783-
dc.description.abstractBoth β1- and α1-adrenoceptors are present on canine coronary arteries, and they are accessible to norepinephrine released from the sympathetic nerves. Under normal conditions, these arteries relax because of the predominance of the β1-adrenoceptors, whereas constriction prevails in the presence of β1-adrenoceptor antagonists. The coronary arteries also have cholinergic nerves. When activated, these nerves release acetylcholine, which acts on muscarinic receptors on the sympathetic nerve terminals to reduce the output of norepinephrine and thereby lessen the relaxation mediated by β1-adrenoceptors. Thus, muscarinic agonists can precipitate coronary artery spasm. If the smooth muscle cells of the coronary arteries become hypoxic, their responsivneness to β-adrenergic stimulation is lost and constrictor responses are exaggerated. Cardiac glycosides prevent the predominance of the β-adrenergic effects of norepinephrine. Therefore, after treatment with ouabain, release of norepinephrine from the sympathetic nerves leads not to relaxation but to further contraction of coronary arteries. The endothelium of the coronary arteries inhibits platelet aggregation by the formation and release of prostacyclin, and it reacts to platelet products by causing relaxation of the underlying smooth muscle. In addition, if any thrombin is formed, it also causes endothelium-mediated relaxation. If the endothelium is damaged, these protective mechanisms are lost. Patients with coronary artery spasm usually have morphologic changes in the artery at the site of the spasm. Platelets can aggregate at this site and release vasoactive substances, which - aided by formation of thrombin - cause contraction. Thus, the blood supply to the myocardium is reduced; the ensuing hypoxia augments the constriction. Acute myocardial ischemia caused by coronary vasospasm may precipitate acute cardiac rhythm disturbances and sudden death by ventricular tachycardia or fibrillation.en_US
dc.languageengen_US
dc.publisherDowden Health Media, Inc. The Journal's web site is located at http://www.mayoclinicproceedings.comen_US
dc.relation.ispartofMayo Clinic Proceedingsen_US
dc.subject.meshAdrenergic Beta-Agonists - Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAnoxia - Complicationsen_US
dc.subject.meshCatsen_US
dc.subject.meshCholinergic Fibers - Physiopathologyen_US
dc.subject.meshCoronary Disease - Etiology - Physiopathologyen_US
dc.subject.meshCoronary Vasospasm - Complications - Drug Therapy - Physiopathologyen_US
dc.subject.meshCoronary Vessels - Drug Effects - Physiopathologyen_US
dc.subject.meshDogsen_US
dc.subject.meshEndothelium - Physiopathologyen_US
dc.subject.meshMuscle, Smooth, Vascular - Physiology - Physiopathologyen_US
dc.subject.meshPhentolamine - Pharmacologyen_US
dc.subject.meshPlatelet Aggregationen_US
dc.subject.meshReceptors, Adrenergic, Alpha - Drug Effects - Physiologyen_US
dc.subject.meshReceptors, Adrenergic, Beta - Physiologyen_US
dc.subject.meshSympathetic Nervous System - Physiopathologyen_US
dc.titleSpasm of the coronary arteries: Causes and consequences (the scientist's viewpoint)en_US
dc.typeArticleen_US
dc.identifier.emailVanhoutte, PM:vanhoutt@hku.hken_US
dc.identifier.authorityVanhoutte, PM=rp00238en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/S0025-6196(12)65280-X-
dc.identifier.pmid2856944-
dc.identifier.scopuseid_2-s2.0-0022005254en_US
dc.identifier.volume60en_US
dc.identifier.issue1en_US
dc.identifier.spage33en_US
dc.identifier.epage46en_US
dc.identifier.isiWOS:A1985AAY4200005-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridShepherd, JT=7401742522en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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