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Beta-adrenergic signaling influence on cardiomyocyte excitation contraction coupling

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Shelby Dahlen

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Description: The downstream targets of protein kinase A (PKA), which is the major effector of beta-adrenergic signaling in cardiomyocytes. PKA activity in cardiomyocytes increases rate of contraction and relaxation (chronotropy and lusitropy), as well as increases the force of contraction (inotropy). This figure also includes two regulators of G protein signaling (RGS) proteins, which accelerate the GTPase activity of the G-alpha subunit, resulting in termination of G protein signaling.

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The downstream targets of protein kinase A (PKA), which is the major effector of beta-adrenergic signaling in cardiomyocytes. PKA activity in cardiomyocytes increases rate of contraction and relaxation (chronotropy and lusitropy), as well as increases the force of contraction (inotropy). This figure also includes two regulators of G protein signaling (RGS) proteins, which accelerate the GTPase activity of the G-alpha subunit, resulting in termination of G protein signaling.

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