Role of β 2 Adrenergic Receptors in Human Atherosclerotic Coronary Arteries

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Abstract
Background— Adrenergic regulation of coronary vasomotion is balanced between α 1 -adrenergic–mediated (α 1 -AR) constriction and β 2 -adrenergic–mediated (β 2 -AR) relaxation. This study aimed at assessing the role of β 2 -ARs in normal, mildly atherosclerotic, and stenotic human coronary arteries. Methods and Results— During intracoronary (IC) infusion of increasing doses of the β 2 -AR agonist salbutamol (0.15, 0.3, and 0.6 μg/min) and the endothelial vasodilator acetylcholine (1, 3, and 10 μg/min), we measured (1) changes in lumen diameter (LD) by quantitative coronary angiography in 34 normal, 55 mildly atherosclerotic, and 42 stenotic coronary artery segments and (2) changes in average peak velocity (APV) and coronary blood flow (CBF) with the use of Doppler flow wire in 11 normal, 10 mildly atherosclerotic, and 11 stenotic coronary arteries. In 6 of 11 stenotic coronary arteries, the protocol was repeated after an IC bolus (12 μg/kg) of the α-adrenergic blocker phentolamine. In 6 of 11 normal coronary arteries, the protocol was repeated after an IC infusion (60 μmol/min) of N G -monomethyl- l -arginine (L-NMMA), a nitric oxide inhibitor. Neither salbutamol IC infusion nor acetylcholine significantly changed heart rate or blood pressure, whereas L-NMMA slightly increased blood pressure. In normal coronary arteries, salbutamol increased LD (LD max %: 11±2, P P P P P P P P P P P P P P P P =NS) and CBF (CBF max %: −10±13, P =NS). In stenotic coronary arteries, acetylcholine significantly reduced LD (LD max %: −15±3, P P P Conclusions— In severely atherosclerotic coronary arteries, β 2 -adrenergic vasodilatation is impaired, and this might contribute to alter the vasomotor balance, further precipitating myocardial ischemia during sympathetic activation.