Abstract
Ca(2+) influx through the L-type Ca(2+) 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 Ca(2+) influx through Ca(v)1.2 and, consequently, cardiomyocyte contractility. Emerging evidence shows that Ca(v)1.2 is regulated by different mechanisms in cardiomyocytes compared to neurons and vascular smooth muscle cells.