TNFα Stimulated ATP-Sensitive Potassium Channels and Attenuated Deoxyglucose and Ca Uptake of H9c2 Cardiomyocytes

Tumor necrosis factor (TNFα) is an inflammatory cytokine that induces programmed cell death in a variety of tissue types, including the heart. Recent experimental data suggest that the TNF expressed within the myocardium in response to environmental injury plays an important role in initiating homeostatic response. The effect of TNFα (10-50 ng/mL) was studied on ⁸⁶Rb efflux, ³H-deoxyglucose uptake, or ⁴⁵Ca uptake in H9c2 cardiomyocytes. TNFα stimulated ⁸⁶Rb efflux from cultures, while 2 μM glibenclamide blocker of ATP-sensitive potassium channels or 20 μM zvad-fmk caspase inhibitor attenuated this effect. TNFα also depressed the stimulatory effect of 80 mM KCl on ⁴⁵Ca uptake in the cardiomyocytes. TNFα inhibited the stimulatory effect of 100 nM insulin on ³H-deoxyglucose uptake. Our findings further suggest that TNFα mediated adaptive and protective effects in the heart during a brief environmental injury.