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Significance Calcium entry initiates contraction in cardiac myocytes, and altered expression of voltage-gated calcium channel 1.2 (CaV 1.2) causes heart failure in mice. Here we show that reducing β-adrenergic regulation of CaV 1.2 by mutation of a PKA site in the C-terminal domain causes age-related heart failure. Dual mutation of a nearby casein-kinase II phosphorylation site accelerated heart failure. The PKA level was increased; PKA-mediated phosphorylation of ryanodine receptor type-2, phospholamban, and troponin-I was increased; the calcium pool in the sarcoplasmic reticulum was increased; and the activity of the calcium-dependent phosphoprotein phosphatase calcineurin was persistently elevated. These changes in mice with a mutation at the PKA site Ser1700 (SA mice) suggest that compensatory mechanisms may initially enhance contractility but eventually cause increased sensitivity to cardiovascular stress and heart failure.

Loss of β-adrenergic–stimulated phosphorylation of Ca V 1.2 channels on Ser1700 leads to heart failure

Loss of β-adrenergic–stimulated phosphorylation of Ca _V 1.2 channels on Ser1700 leads to heart failure