Role of β2 adrenergic receptors in human atherosclerotic coronary arteries

Emanuele Barbato, Federico Piscione, Jozef Bartunek, Gennaro Galasso, Plinio Cirillo, Giuseppe De Luca, Guido Iaccarino, Bernard De Bruyne, Massimo Chiariello, William Wijns

Research output: Contribution to journalArticle

52 Citations (Scopus)

Abstract

Background - Adrenergic regulation of coronary vasomotion is balanced between α1-adrenergic-mediated (α1-AR) constriction and β2-adrenergic-mediated (β2-AR) relaxation. This study aimed at assessing the role of β2-ARs in normal, mildly atherosclerotic, and stenotic human coronary arteries. Methods and Results - During intracoronary (IC) infusion of increasing doses of the β2-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 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, P2-adrenergic vasodilatation is impaired, and this might contribute to alter the vasomotor balance, further precipitating myocardial ischemia during sympathetic activation.

Original languageEnglish
Pages (from-to)288-294
Number of pages7
JournalCirculation
Volume111
Issue number3
DOIs
Publication statusPublished - Jan 25 2005

Fingerprint

Adrenergic Receptors
Coronary Vessels
Adrenergic Agents
Albuterol
omega-N-Methylarginine
Acetylcholine
Blood Pressure
Adrenergic Agonists
Adrenergic Antagonists
Blood Flow Velocity
Phentolamine
Coronary Angiography
Vasodilator Agents
Constriction
Vasodilation
Myocardial Ischemia
Nitric Oxide
Heart Rate

Keywords

  • Acetylcholine
  • Atherosclerosis
  • Endothelium
  • Receptors, adrenergic, alpha
  • Receptors, adrenergic, beta

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine

Cite this

Barbato, E., Piscione, F., Bartunek, J., Galasso, G., Cirillo, P., De Luca, G., ... Wijns, W. (2005). Role of β2 adrenergic receptors in human atherosclerotic coronary arteries. Circulation, 111(3), 288-294. https://doi.org/10.1161/01.CIR.0000153270.25541.72

Role of β2 adrenergic receptors in human atherosclerotic coronary arteries. / Barbato, Emanuele; Piscione, Federico; Bartunek, Jozef; Galasso, Gennaro; Cirillo, Plinio; De Luca, Giuseppe; Iaccarino, Guido; De Bruyne, Bernard; Chiariello, Massimo; Wijns, William.

In: Circulation, Vol. 111, No. 3, 25.01.2005, p. 288-294.

Research output: Contribution to journalArticle

Barbato, E, Piscione, F, Bartunek, J, Galasso, G, Cirillo, P, De Luca, G, Iaccarino, G, De Bruyne, B, Chiariello, M & Wijns, W 2005, 'Role of β2 adrenergic receptors in human atherosclerotic coronary arteries', Circulation, vol. 111, no. 3, pp. 288-294. https://doi.org/10.1161/01.CIR.0000153270.25541.72
Barbato E, Piscione F, Bartunek J, Galasso G, Cirillo P, De Luca G et al. Role of β2 adrenergic receptors in human atherosclerotic coronary arteries. Circulation. 2005 Jan 25;111(3):288-294. https://doi.org/10.1161/01.CIR.0000153270.25541.72
Barbato, Emanuele ; Piscione, Federico ; Bartunek, Jozef ; Galasso, Gennaro ; Cirillo, Plinio ; De Luca, Giuseppe ; Iaccarino, Guido ; De Bruyne, Bernard ; Chiariello, Massimo ; Wijns, William. / Role of β2 adrenergic receptors in human atherosclerotic coronary arteries. In: Circulation. 2005 ; Vol. 111, No. 3. pp. 288-294.
@article{96e30b483a0c4f6f8a613123c7c00039,
title = "Role of β2 adrenergic receptors in human atherosclerotic coronary arteries",
abstract = "Background - Adrenergic regulation of coronary vasomotion is balanced between α1-adrenergic-mediated (α1-AR) constriction and β2-adrenergic-mediated (β2-AR) relaxation. This study aimed at assessing the role of β2-ARs in normal, mildly atherosclerotic, and stenotic human coronary arteries. Methods and Results - During intracoronary (IC) infusion of increasing doses of the β2-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 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, P2-adrenergic vasodilatation is impaired, and this might contribute to alter the vasomotor balance, further precipitating myocardial ischemia during sympathetic activation.",
keywords = "Acetylcholine, Atherosclerosis, Endothelium, Receptors, adrenergic, alpha, Receptors, adrenergic, beta",
author = "Emanuele Barbato and Federico Piscione and Jozef Bartunek and Gennaro Galasso and Plinio Cirillo and {De Luca}, Giuseppe and Guido Iaccarino and {De Bruyne}, Bernard and Massimo Chiariello and William Wijns",
year = "2005",
month = "1",
day = "25",
doi = "10.1161/01.CIR.0000153270.25541.72",
language = "English",
volume = "111",
pages = "288--294",
journal = "Circulation",
issn = "0009-7322",
publisher = "Lippincott Williams and Wilkins",
number = "3",

}

TY - JOUR

T1 - Role of β2 adrenergic receptors in human atherosclerotic coronary arteries

AU - Barbato, Emanuele

AU - Piscione, Federico

AU - Bartunek, Jozef

AU - Galasso, Gennaro

AU - Cirillo, Plinio

AU - De Luca, Giuseppe

AU - Iaccarino, Guido

AU - De Bruyne, Bernard

AU - Chiariello, Massimo

AU - Wijns, William

PY - 2005/1/25

Y1 - 2005/1/25

N2 - Background - Adrenergic regulation of coronary vasomotion is balanced between α1-adrenergic-mediated (α1-AR) constriction and β2-adrenergic-mediated (β2-AR) relaxation. This study aimed at assessing the role of β2-ARs in normal, mildly atherosclerotic, and stenotic human coronary arteries. Methods and Results - During intracoronary (IC) infusion of increasing doses of the β2-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 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, P2-adrenergic vasodilatation is impaired, and this might contribute to alter the vasomotor balance, further precipitating myocardial ischemia during sympathetic activation.

AB - Background - Adrenergic regulation of coronary vasomotion is balanced between α1-adrenergic-mediated (α1-AR) constriction and β2-adrenergic-mediated (β2-AR) relaxation. This study aimed at assessing the role of β2-ARs in normal, mildly atherosclerotic, and stenotic human coronary arteries. Methods and Results - During intracoronary (IC) infusion of increasing doses of the β2-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 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, P2-adrenergic vasodilatation is impaired, and this might contribute to alter the vasomotor balance, further precipitating myocardial ischemia during sympathetic activation.

KW - Acetylcholine

KW - Atherosclerosis

KW - Endothelium

KW - Receptors, adrenergic, alpha

KW - Receptors, adrenergic, beta

UR - http://www.scopus.com/inward/record.url?scp=19944431741&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=19944431741&partnerID=8YFLogxK

U2 - 10.1161/01.CIR.0000153270.25541.72

DO - 10.1161/01.CIR.0000153270.25541.72

M3 - Article

C2 - 15642763

AN - SCOPUS:19944431741

VL - 111

SP - 288

EP - 294

JO - Circulation

JF - Circulation

SN - 0009-7322

IS - 3

ER -