The β 2 -Adrenergic Receptor Delivers an Antiapoptotic Signal to Cardiac Myocytes Through G i -Dependent Coupling to Phosphatidylinositol 3′-Kinase

Abstract
—Recent studies have shown that chronic β-adrenergic receptor (β-AR) stimulation alters cardiac myocyte survival in a receptor subtype-specific manner. We examined the effect of selective β1- and β2-AR subtype stimulation on apoptosis induced by hypoxia or H2O2 in rat neonatal cardiac myocytes. Although neither β1- nor β2-AR stimulation had any significant effect on the basal level of apoptosis, selective β2-AR stimulation protected myocytes from apoptosis. β2-AR stimulation markedly increased mitogen-activated protein kinase/extracellular signal–regulated protein kinase (MAPK/ERK) activation as well as phosphatidylinositol-3′-kinase (PI-3K) activity and Akt/protein kinase B phosphorylation. β1-AR stimulation also markedly increased MAPK/ERK activation but only minimally activated PI-3K and Akt. Pretreatment with pertussis toxin blocked β2-AR–mediated protection from apoptosis as well as the β2-AR–stimulated changes in MAPK/ERK, PI-3K, and Akt/protein kinase B. The selective PI-3K inhibitor, LY 29...

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