Inhibition of protein kinase Cα improves myocardial β-adrenergic receptor signaling and ventricular function in a model of myocardial preservation

Current techniques of myocardial preservation are associated with inhibition of protein kinase Cα activity and maintenance of intact β-adrenergic receptor signaling. Activation of protein kinase Cα leads to enhanced β-adrenergic receptor desensitization and impaired signaling and ventricular function as a result of increased G protein-coupled receptor kinase 2 activity. This is a novel in vivo mechanism of G protein-coupled receptor kinase 2 activation. Strategies to specifically inhibit these kinases might improve long-term myocardial protection.