Impact of neuroendocrine activation on coronary artery disease.
Several independent predictors of the risk of atherosclerosis are known including plasma cholesterol concentration, cigarette smoking, elevated blood pressure, as well as genetic factors such as non-insulin-dependent diabetes and plasma fibrinogen. Also known are the 3 major elements of the pathogenesis of atherosclerosis, involving modification of endothelial function, changes in vascular tone, and clinical sequelae of hyperplasia of smooth muscle cells in the intima of the affected blood vessels. This article further examines vasoconstrictor/vasodilator balance, the role of angiotensin II, and the significant role played by the endothelium in the complex events and interactions that occur both with smooth muscle cells and platelets. Clinical evidence of endothelial dysfunction in coronary artery disease is presented. The importance of the association of the progression of coronary artery disease with signs of neuroendocrine activation, the relation of endothelin-1 to mechanisms of neuroendocrine activation, and how the counteraction of this activation may have beneficial effects on disease progression are discussed.
Swedberg
K B
KB
Department of Medicine, Sahlgrenska University Hospital/Ostra, Göteborg, Sweden.
D000804:Angiotensin II / Q000378:metabolism; D003327:Coronary Disease / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D003331:Coronary Vessels / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D016232:Endothelins / Q000378:metabolism; D004730:Endothelium, Vascular / Q000378:metabolism / Q000503:physiopathology; D006801:Humans; D009131:Muscle, Smooth, Vascular / Q000378:metabolism / Q000503:physiopathology; D009490:Neurosecretory Systems / Q000378:metabolism / Q000503:physiopathology*; D012084:Renin-Angiotensin System / Q000502:physiology; D014661:Vasoconstriction
D016232:Endothelins; D000804:Angiotensin II