Activation of cardiac beta 2 adrenoceptors in the human heart.

Comparative pharmacologic studies have indicated that the cardiac beta 2 adrenoceptors of vertebrate species are "adrenaline" receptors; i.e., the distribution of beta 2 receptors in the heart seems to be related to the amounts of adrenaline in the sympathetic nerves and in the circulation, and the beta 2 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 beta 2 receptors. These findings are in agreement with radioligand binding studies demonstrating up to 50% beta 2 receptors in myocardial membrane preparations. The pharmacologic studies thus add support to the assumption that these beta 2 receptors are functionally active and not merely experimental oddities. It is hypothesized that in normal situations the beta 2-receptor effects are additive to the beta 1 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 beta 2 receptors. It is postulated that only unselective beta blockers can abolish all beta-receptor effects in the heart during stress reactions with profound catecholamine stimulation.