(Circulation. 2000;101:689.)
© 2000 American Heart Association, Inc.
From Bench to Bedside |
-Adrenergic Coronary Vasoconstriction and Myocardial Ischemia in Humans
From Abteilung für Pathophysiologie (G.H.) and Abteilung für Kardiologie (D.B.), Universitätsklinikum Essen, Essen, Germany; MRC Cyclotron Unit, Imperial College School of Medicine, Hammersmith Hospital, London, UK (P.C., O.R.); Department of Physiology, Medical College of Wisconsin, Milwaukee (W.C.); Centro di Fisiologia Clinica, Ospedale Maggiore IRCCS, Milano, Italy (L.G.); Kardiologie, Universitätsspital Bern, Switzerland (O.H.); and Cattedra di Cardiologia, Università Federico II, Napoli, Italy (C.I.).
Correspondence to Prof Dr Gerd Heusch, Direktor der Abteilung für Pathophysiologie, Zentrum für Innere Medizin, Universitätsklinikum Essen, Hufelandstraße 55, 45122 Essen, Germany. E-mail gerd.heusch{at}uni-essen.de
Abstract
Abstract—The use of quantitative
coronary angiography, combined with Doppler and PET, has
recently been directed at the study of 
-adrenergic coronary
vasomotion in humans. Confirming prior animal experiments, there is no
evidence of -adrenergic coronary constrictor tone at rest.
Again confirming prior experiments, responses to -adrenoceptor
activation are augmented in the presence of coronary
endothelial dysfunction and
atherosclerosis, involving both 1- and
2-adrenoceptors in epicardial conduit arteries and
microvessels. Such augmented -adrenergic coronary
constriction is observed during exercise and coronary
interventions, and it is powerful enough to induce myocardial
ischemia and limit myocardial function. Recent studies indicate
a genetic determination of 2-adrenergic coronary
constriction.
Key Words: coronary disease • ischemia • microcirculation • nervous system • receptors, adrenergic, alpha
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