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Recent Advances in Cardiac ß2-Adrenergic Signal Transduction
From the Laboratory of Cardiovascular Science, Gerontology Research Center, National Institute on Aging, Baltimore, Md.
Correspondence to Rui-Ping Xiao, MD, PhD, Laboratory of Cardiovascular Science, Gerontology Research Center, National Institute on Aging, 5600 Nathan Shock Dr, Baltimore, MD 21224. E-mail XiaoR{at}grc.nia.nih.gov
Abstract—Recent studies have added complexities to the conceptual framework of cardiac ß-adrenergic receptor (ß-AR) signal transduction. Whereas the classical linear Gs–adenylyl cyclase–cAMP–protein kinase A (PKA) signaling cascade has been corroborated for ß1-AR stimulation, the ß2-AR signaling pathway bifurcates at the very first postreceptor step, the G protein level. In addition to Gs, ß2-AR couples to pertussis toxin–sensitive Gi proteins, Gi2 and Gi3. The coupling of ß2-AR to Gi proteins mediates, to a large extent, the differential actions of the ß-AR subtypes on cardiac Ca2+ handling, contractility, cAMP accumulation, and PKA-mediated protein phosphorylation. The extent of Gi coupling in ventricular myocytes appears to be the basis of the substantial species-to-species diversity in ß2-AR–mediated cardiac responses. There is an apparent dissociation of ß2-AR–induced augmentations of the intracellular Ca2+ (Cai) transient and contractility from cAMP production and PKA-dependent cytoplasmic protein phosphorylation. This can be largely explained by Gi-dependent functional compartmentalization of the ß2-AR–directed cAMP/PKA signaling to the sarcolemmal microdomain. This compartmentalization allows the common second messenger, cAMP, to perform selective functions during ß-AR subtype stimulation. Emerging evidence also points to distinctly different roles of these ß-AR subtypes in modulating noncontractile cellular processes. These recent findings not only reveal the diversity and specificity of ß-AR and G protein interactions but also provide new insights for understanding the differential regulation and functionality of ß-AR subtypes in healthy and diseased hearts.
Key Words: ß-adrenergic receptor subtype • G protein • cAMP compartmentalization • heart failure
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