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The oxygen delivered by the coronary blood flow at rest is almost maximally extracted (nearly 75%) by the heart. This implies a very limited oxygen extraction reserve of the myocardium. Therefore, the increase in oxygen consumption occurring during exercise can only happen at the cost of an increase in oxygen delivery provided by an augmented coronary blood flow. This increase in flow is mediated through local metabolic mechanisms and partially through adrenergic receptor mediated vasomotion. This review will focus specifically on the role played by the vascular adrenergic receptors in the modulation of coronary vasomotion.
Adrenergic modulation of coronary blood flow is the result of a complex balance between receptors mostly acting as vasoconstrictors (α-adrenergic receptors) and receptors mostly acting as vasodilators (β-adrenergic receptors) (fig 1). The presence of two subtypes of α-adrenergic receptors (α-ARs) has been demonstrated in coronary arteries: α1-ARs and α2-ARs.1 2 Both these receptors are located on vascular smooth muscle cells and mediate coronary vasoconstriction. These receptors are not uniformly distributed in the coronary circulation: α1-adrenoceptors are predominant in larger vessels and α2-adrenoceptors are predominant in the microcirculation. α2-adrenergic receptors have also been demonstrated on endothelial cells, where they have been associated with vasorelaxation through nitric oxide (NO) release.
Three β-adrenergic receptor (β-AR) subtypes have been demonstrated in the coronary circulation: β1-ARs, β2-ARs and β3-ARs.2–4 The smaller the coronary arteries, the higher the density of the β-adrenergic receptors: a fivefold greater density of β-adrenergic receptors has been found in arterioles as compared with small and medium sized arteries and a 34-fold greater density …