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Introduction: Metabolic stress is observed in clinical and experimental atrial fibrillation (AF). Metabolic stress activates AMP-dependent protein kinase (AMPK) via phosphorylation; activated AMPK produces compensatory changes in the determinants of energy balance. Here, we examined AMPK responses in AF and their role in remodeling responses of atrial Ca²⁺ handling and contractility.

Methods: AMPK and Cav1.2 protein were quantified by immunoblot. Ca²⁺ transients (CaTs, Indo1 AM), cell shortening (CS, videometry), L-type Ca²⁺ (I_Ca,L) and NCX (I_NCX) current (patch clamp) were measured in dog left atrial (LA) cardiomyocytes (CMs) under metabolic stress due to glycolysis inhibition (GI, 10 mM 2-deoxyglucose/10 mM pyruvate).

Results: In dogs with 1-wk electrically-maintained AF (n=4), the phosphorylation ratio (PhR) of AMPK (indicating activation) increased in LA by 101%* (*p<0.05) vs. controls (n=4 …