ATP-Sensitive Potassium Channel Currents in Eccentrically Hypertrophied Cardiac Myocytes of Volume-Overloaded Rats.

ATP-sensitive potassium channels (K(ATP)) protect the myocardium from hypertrophy induced by pressure-overloading. In this study, we determined the effects of these channels in volume-overloading. We compared the effects of a K(ATP) agonist and a K(ATP) antagonist on sarcolemmal transmembrane current density (pA/pF) clamped at 20 mV increments of membrane potential from -80 to +40 mV in ventricular cardiac myocytes. The basal outward potassium pA/pF in myocytes of volume-overloaded animals was significantly smaller than that in the myocytes of sham-operated controls. Treatment of the control myocytes with the K(ATP) agonist cromakalim increased pA/pF significantly. This increase was blocked by the K(ATP) antagonist glibenclamide. Treatment of the hypertrophied myocytes from volume-overloaded animals with cromakalim and in the presence and absence of glibenclamide did not change pA/pF significantly. These findings suggest that eccentrically hypertrophied cardiac myocytes from volume-overloading may be unresponsive to specific activation/inactivation of K(ATP) and that dysfunctional K(ATP) may fail to protect the myocardium from left ventricular hypertrophy associated with volume-overloading.