Tissue-specific adrenergic regulation of the L-type Ca2+ channel CaV1.2

Abstract

Ca2+ influx through the L-type Ca2+ channel Cav1.2 triggers each heartbeat. The fight-or-flight response induces the release of the stress response hormone norepinephrine to stimulate β-adrenergic receptors, cAMP production, and protein kinase A activity to augment Ca2+ influx through Cav1.2 and, consequently, cardiomyocyte contractility. Emerging evidence shows that Cav1.2 is regulated by different mechanisms in cardiomyocytes compared to neurons and vascular smooth muscle cells.