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Significance This work defines the in vivo role of phosphorylation of Ser1700 and Thr1704 in CaV 1.2 channels in the fight-or-flight response. Mutation of both residues to Ala in STAA mice reduced basal L-type Ca2+ currents and markedly decreased β-adrenergic stimulation of Ca2+ currents and cell contraction. STAA ventricular myocytes exhibited arrhythmic contractions and often failed to sustain contractions when stimulated at 1 Hz. STAA mice have reduced exercise capacity, and cardiac hypertrophy is evident at 3 mo. Our results define the molecular mechanism for Ca2+ channel regulation in the fight-or-flight response and give insight into mechanisms that underlie cardiac homeostasis and hypertrophy.

Phosphorylation sites required for regulation of cardiac calcium channels in the fight-or-flight response