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Background —β-Adrenergic receptor (β-AR) stimulation increases apoptosis in adult rat cardiac (ventricular) myocytes (ARVMs) via activation of adenylyl cyclase. β2 -ARs may couple to a Gi -mediated signaling pathway that can oppose the actions of adenylyl cyclase.Methods and Results —In ARVMs, β-AR stimulation for 24 hours increased the number of apoptotic cells as measured by flow cytometry. β-AR–stimulated apoptosis was abolished by the β1 -AR–selective antagonist CGP 20712A (P &lt;0.05 versus β-AR stimulation alone) but was potentiated by the β2 -AR–selective antagonist ICI 118,551 (P &lt;0.05 versus β-AR stimulation alone). The muscarinic agonist carbachol also prevented β-AR–stimulated apoptosis (P &lt;0.05 versus β-AR stimulation alone), whereas pertussis toxin potentiated the apoptotic action of β-AR stimulation (P &lt;0.05 versus β-AR stimulation alone) and prevented the antiapoptotic action of carbachol.Conclusions —In ARVMs, stimulation of β1 -ARs increases apoptosis via a cAMP-dependent mechanism, whereas stimulation of β2 -ARs inhibits apoptosis via a Gi -coupled pathway. These findings have implications for the pathophysiology and treatment of myocardial failure.

Opposing Effects of β 1 - and β 2 -Adrenergic Receptors on Cardiac Myocyte Apoptosis

Opposing Effects of β ₁ - and β ₂ -Adrenergic Receptors on Cardiac Myocyte Apoptosis