New insights into the cellular mechanisms of vasospasm.
Previous attempts to define the etiology of coronary artery spasm have focused on such mechanisms as autonomic nervous system dysfunction or enhanced platelet activation leading to high levels of circulating vasoconstrictors. More recent evidence, however, suggests that the basic abnormality may be hypercontractility of the arterial wall associated with the atherosclerotic process itself. Results of both animal experiments and clinical studies support a role for certain cellular events in atherogenesis, including endothelial injury, presence of mitogenic factors and leukotrienes generated by platelets and macrophages, changes in histamine and serotonin receptor density of vascular smooth muscle and neovascularization of atherosclerotic plaque. The mechanisms postulated to underlie coronary vasospasm are discussed, relative to the clinical characteristics of vasospastic angina and the possible therapeutic implications.
D000818:Animals; D001161:Arteriosclerosis / Q000209:etiology / Q000473:pathology / Q000503:physiopathology*; D001341:Autonomic Nervous System / Q000503:physiopathology; D001792:Blood Platelets / Q000502:physiology; D003329:Coronary Vasospasm / Q000209:etiology / Q000473:pathology / Q000503:physiopathology*; D003331:Coronary Vessels / Q000473:pathology*; D004727:Endothelium / Q000473:pathology; D006801:Humans; D008264:Macrophages / Q000502:physiology; D009119:Muscle Contraction; D009131:Muscle, Smooth, Vascular / Q000503:physiopathology; D011817:Rabbits; D051381:Rats; D011969:Receptors, Histamine H1 / Q000502:physiology; D011985:Receptors, Serotonin / Q000502:physiology; D014651:Vasa Vasorum / Q000503:physiopathology; D014661:Vasoconstriction
D011969:Receptors, Histamine H1; D011985:Receptors, Serotonin