Opposing Effects of β₁- and β₂-Adrenergic Receptors on Cardiac Myocyte Apoptosis

Abstract

In ARVMs, stimulation of beta(1)-ARs increases apoptosis via a cAMP-dependent mechanism, whereas stimulation of beta(2)-ARs inhibits apoptosis via a G(i)-coupled pathway. These findings have implications for the pathophysiology and treatment of myocardial failure.