The paradox of α-adrenergic coronary vasoconstriction revisited

Activation of coronary vascular α-adrenoceptors results in vasoconstriction which competes with metabolic vasodilation during sympathetic activation. Epicardial conduit vessel constriction is largely mediated by α1-adrenoceptors; the constriction of the resistive microcirculation largely by α2-adrenoceptors, but also by α1-adrenoceptors. There is no firm evidence that α-adrenergic coronary vasoconstriction exerts a beneficial effect on transmural blood flow distribution. In fact, α-blockade in anesthetized and conscious dogs improves blood flow to all transmural layers, during normoperfusion and hypoperfusion. Also, in patients with coronary artery disease, blockade of α1- and α2-adrenoceptors improves coronary blood flow, myocardial function and metabolism.

Research highlights
► The coronary circulation has α1– and α2-adrenoceptors.
► α-Adrenergic coronary vasoconstriction competes with metabolic and endothelium-dependent vasodilation.
► α-Adrenoceptor blockade improves blood flow to all transmural layers.
► The dog coronary circulation is a good model for the human coronary circulation.
► Adrenoceptor blockade improves blood coronary blood flow and attenuates ischemia in patients.