Neuronal control of coronary blood flow

Abstract

Controversies on acetylcholine-induced increases or decreases in coronary blood flow arise from obvious species differences, the role of endothelium in mediating vascular smooth muscle responses, and the marked negative chronotropic and inotropic effects of acetylcholine. In man, there appears to be a predominant dilation of intact epicardial coronary arteries and a constriction of artherosclerotic segments. However, at present there is no evidence for a vagal initiation of myocardial ischemia. Coronary vascular beta-adrenergic receptors mediate dilation, but appear to be functionally insignificant during sympathetic activation. The beta-adrenergic mechanism contributing to myocardial ischemia are indirect, mediated by a tachycardia-related redistribution of blood flow away from the ischemic myocardium. alpha-Adrenergic receptors mediating epicardial coronary artery constriction in experimental studies appear not to be responsible for the initiation of ischemia in patients with angina at rest. However, alpha-adrenergic constriction of coronary resistance vessels resulting in the precipitation of post-stenotic myocardial ischemia was demonstrated in experimental studies and recently confirmed in patients with effort angina. Non-adrenergic, non-cholinergic neurotransmitters exist; however, their role in regulating coronary blood flow remains entirely unclear.

Inhibition of centrally induced ventricular arrhythmias by rilmenidine and idazoxan in rabbits

“…The anti-arrhythmic effects and/or antiischaemic effects of idazoxan and other drugs with alpha2-adrenoceptor antagonist activity have been suggested to be mediated through the blockade of peripheral postsynaptic alpha-adrenergic receptors in the heart and blood vessels (Segal et al 1981(Segal et al , 1984Seitelberger et al 1991;Baumgart and Heusch 1995;Roegel et al 1996). Stimulation of alpha2-adrenergic receptors also induces coronary constriction during stress and cardiac ischemia (Seitelberger et al 1991;Baumgart and Heusch 1995). So, idazoxan might prevent the bicuculline-induced vasoconstriction by blocking postsynaptic alphaz-adrenergic receptors, in particular in the coronary arteries.…”

Location and variability of epicardiac ganglia in human fetuses

“…Intrinsic cardiac nervous system (ICNS) plays a crucial role in regulation of heart rate, contractility and tone of the coronary vessels (Young et al 1987;Ardel 1994;Baumgart and Heusch 1995;Furukawa et al 1997;Dickerson et al 1998;Feigl 1998;Tsuboi et al 2000;Randall et al 2003;Olufsen et al 2005). In neonates and infants, the intrinsic neural pathways are considered to be important for radiofrequency ablation that is performable in cases of incessant supraventricular and atrioventricular nodal re-entry tachycardia (Osborn et al 1999;Blaufox et al 2001;Shah et al 2001;Oudijk et al 2003;Van Hare et al 2004).…”

Postexercise Ischemia Is Associated With Increased Neuropeptide Y in Patients With Coronary Artery Disease

“…The release of norepinephrine (NE) leads to increased myocardial oxygen demand via a ␤-adrenoceptor-mediated increased heart rate (HR) and contractility, as well as limitation of the increase in oxygen supply due to an ␣-adrenoceptor-mediated coronary vasoconstriction. 1 Earlier studies suggest a significant role of ␣-adrenergic coronary vasoconstriction during exerciseinduced myocardial ischemia in patients with stable angina pectoris. 1,2 However, it remains unknown whether the nonadrenergic sympathetic cotransmitter neuropeptide Y (NPY) contributes.…”

“…1 Earlier studies suggest a significant role of ␣-adrenergic coronary vasoconstriction during exerciseinduced myocardial ischemia in patients with stable angina pectoris. 1,2 However, it remains unknown whether the nonadrenergic sympathetic cotransmitter neuropeptide Y (NPY) contributes.…”