Abstract
We review the role of endothelin (ET) A-receptors (R) on the coronary circulation. ET-1 maintains the normal coronary artery tone. ET-1 plasma levels are increased during and after coronary angioplasty and this increase is related to myocardial ischaemia rather than to mechanical artery injury. ETAR antagonists inhibit coronary artery vasoconstriction induced by ET release after coronary angioplasty in humans. ET promotes neointimal formation and ETAR antagonism has been shown to inhibit restenosis after angioplasty in the animal model but not in humans. ETAR blockade increases coronary blood flow, dilates distal coronary arterial segments and decreases coronary vascular resistance. Coronary collaterals are less sensitive than other coronary vessels to ET-1. ETAR blockade decreases collateral blood flow and, consequently, perfusion of the ischemic myocardium.
Highlights
Diseases of the cardiovascular system account for the majority of morbidity and mortality in Western countries
In a study utilizing the selective ETAR antagonist BQ-123 in patients undergoing angioplasty [14], acute ETAR receptor antagonism prevented the normal reducetion of myocardial ischemia on repeated balloon inflations
This phenomenon may be explained by a “steal” effect through coronary collaterals; local ETAR receptor antagonism with BQ-123 causes coronary vasodilatation, an increase in coronary blood flow, and a decrease in the coronary artery resistance [14] (Figure 3)
Summary
Diseases of the cardiovascular system account for the majority of morbidity and mortality in Western countries. When the coronary flow was reduced to an ischemic level, ET-1 secretion rates into effluent decreased by 60%, but increased 3- to 4-fold after reperfusion at normal flow These data do not support a vasoconstrictor action of ET-1 in rats following ischemia/reperfusion, but rather point to a possible vasodilator role of the peptide under these conditions. Biopsies from internal mammary arteries in patients undergoing coronary artery by-pass grafting showed that systemic hypertension is associated with increased ET-1 and ETAR receptor mRNA expression, whereas insulin-dependent diabetes down-regulates ETAR receptor mRNA expression [13]. This could help explain the differential response of hypertensive and diabetic animals and humans to external and internal stimulation and blockade of ET-1 and its receptors
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