Activation of cardiac beta2 adrenoceptors in the human heart

Comparative pharmacologic studies have indicated that the cardiac β2 adrenoceptors of vertebrate species are “adrenaline” receptors; i.e., the distribution of β2 receptors in the heart seems to be related to the amounts of adrenaline in the sympathetic nerves and in the circulation, and the β2 receptors seem to be stimulated mainly by adrenaline. In the human right atrium the order of potency for the agonists and the blocking agents indicate a relatively high proportion of active β2 receptors. These findings are in agreement with radioligand binding studies demonstrating up to 50% β2 receptors in myocardial membrane preparations. The pharmacologic studies thus add support to the assumption that these β2 receptors are functionally active and not merely experimental oddities. It is hypothesized that in normal situations the β2-receptor effects are additive to the β1 effects. However, during acute stress situations the large amounts of released adrenaline are assumed to increase markedly both inotropy and chronotropy in the heart via β2 receptors. It is postulated that only unselective β blockers can abolish all β-receptor effects in the heart during stress reactions with profound catecholamine stimulation.