on January 10, 2005
Published online before print January 10, 2005, doi: 10.1161/01.CIR.0000153270.25541.72
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Submitted on June 19, 2004
From the Divisions of Cardiology (E.B., F.P., G.G., P.C., G.D.L., M.C.) and Internal Medicine (G.I.), Federico II University of Naples, Italy; and the Cardiovascular Center OLVZ, Aalst, Belgium (E.B., J.B., B.D.B., W.W.). * To whom correspondence should be addressed. E-mail: piscione{at}unina.it.
Background--Adrenergic regulation of coronary vasomotion is balanced between Methods and Results--During intracoronary (IC) infusion of increasing doses of the Conclusions--In severely atherosclerotic coronary arteries,
Revised on October 8, 2004
Accepted on October 21, 2004
Role of
Emanuele Barbato MD, 
2 Adrenergic Receptors in Human Atherosclerotic Coronary Arteries
1-adrenergic-mediated (1-AR) constriction and 
2-adrenergic-mediated (2-AR) relaxation. This study aimed at assessing the role of 2-ARs in normal, mildly atherosclerotic, and stenotic human coronary arteries.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 -adrenergic blocker phentolamine. In 6 of 11 normal coronary arteries, the protocol was repeated after an IC infusion (60 µmol/min) of NG-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<0.05), APV (APV max %: 53±17, P<0.05), and CBF (CBF max %: 57±17, P<0.05), whereas L-NMMA caused a blunted APV (APV max %: 27±6, P<0.05) and CBF (CBF max %: 29±6, P<0.05) response to salbutamol. In mildly atherosclerotic coronary arteries, the salbutamol increase in LD (LD max %: 10±2, P<0.05), APV (APV max %: 33±12, P<0.05), and CBF (CBF max %: 37±12, P<0.05) was preserved. In stenotic coronary arteries, salbutamol induced a paradoxical reduction in LD (LD max %: -6±2, P<0.05), APV (APV max %: -15±9, P<0.05), and CBF (CBF max %: -15±6, P<0.05), which was no longer observed after phentolamine. Acetylcholine increased LD (LD max %: 14±3, P<0.05), APV (APV max %: 61±20, P<0.05), and CBF (CBF max %: 67±19, P<0.05) in normal coronary arteries. In mildly atherosclerotic coronary arteries, acetylcholine induced a significant reduction in LD (LD max %: -15±2, P<0.05) and no changes in APV (APV max %: -6±13, P=NS) and CBF (CBF max %: -10±13, P=NS). In stenotic coronary arteries, acetylcholine significantly reduced LD (LD max %: -15±3, P<0.05), APV (APV max %: -15±9, P<0.05), and CBF (CBF max %: -15±6, P<0.05).2-adrenergic vasodilatation is impaired, and this might contribute to alter the vasomotor balance, further precipitating myocardial ischemia during sympathetic activation.
Key words: receptors, adrenergic, alpha • receptors, adrenergic, beta • atherosclerosis • endothelium • acetylcholine
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