Metabolic stress in guinea pig cardiomyocytes initiated cyclical activation of ATP-sensitive potassium currents and suppressed calcium transients, driven by glycolytic oscillations.
Energy-driven oscillations in potassium currents produce cyclical changes in the cardiac action potential, which may contribute to the genesis of arrhythmias during metabolic compromise.
Periodic changes in membrane ionic current linked to intrinsic oscillations of energy metabolism were identified in guinea pig cardiomyocytes. Metabolic stress initiated cyclical activation of adenosine triphosphate-sensitive potassium current and concomitant suppression of depolarization-evoked intracellular calcium transients. The oscillations in membrane current and excitation-contraction coupling were linked to oscillations in the oxidation state of pyridine nucleotides but were not driven by pacemaker currents or alterations in the concentration of cytosolic calcium. Interventions that altered the rate of glucose metabolism modulated the oscillations, suggesting that the rhythms originated at the level of glycolysis. The energy-driven oscillations in potassium currents produced cyclical changes in the cardiac action potential and thus may contribute to the genesis of arrhythmias during metabolic compromise.
O’Rourke et al. (1994) studied Metabolic compromise. Metabolic stress was evaluated on Oscillations in membrane current and excitation-contraction coupling. Metabolic stress in guinea pig cardiomyocytes initiated cyclical activation of ATP-sensitive potassium currents and suppressed calcium transients, driven by glycolytic oscillations.