Catecholamine-induced coronary vasodilatation is primarily driven by increased myocardial oxygen consumption rather than direct beta-adrenergic receptor stimulation, which plays a minor physiological role.
Do coronary blood vessels contain an intrinsic adrenergic mechanism for vasodilatation of physiological significance?
Adrenergic beta-receptors exist in coronary vessels and mediate vasodilatation, but this effect is physiologically minor compared to vasodilatation driven by myocardial oxygen consumption.
The question of whether the coronary blood vessels contain an intrinsic adrenergic mechanism for vasodilatation of physiological significance has been examined in the canine heart-lung preparation with a donor by studying the response of the coronary vessels to epinephrine, norepinephrine, isoproterenol and salbutamol in combination with practolol. To differentiate the vasodilatation mediated through adrenoceptors in the coronary vessels from that resulting from an increase in the myocardial O2 consumption, a special method of analysis was developed based on the linear relation between the coronary flow and the myocardial O2 consumption. It was found that all four compounds produced an increase in the coronary flow attributable to an increased myocardial O2 consumption. Epinephrine and norepinephrine produced a decrease in the coronary flow after practolol which completely abolished the increase in the myocardial O2 consumption as well as the positive inotropic and chronotropic effects produced by these compounds, while isoproterenol and salbutamol produced an increase. These results indicate that adrenergic beta-receptor exists in the coronary subserving a vasodilatation. However, the vasodilatation through this mechanism is of minor importance under physiological conditions and becomes completely masked in the presence of an overwhelmingly strong vasodilatation consequent to an increase in the myocardial O2 consumption.
Imai et al. (Wed,) conducted a other in Healthy (animal model). Catecholamines (epinephrine, norepinephrine, isoproterenol, salbutamol) vs. Baseline and adrenergic blockade (practolol, phentolamine) was evaluated on Relationship between coronary blood flow and myocardial oxygen consumption. Catecholamine-induced coronary vasodilatation is primarily driven by increased myocardial oxygen consumption rather than direct beta-adrenergic receptor stimulation, which plays a minor physiological role.
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