Electrophysiological response of rat ventricular myocytes to acidosis.

The effects of acidosis on the action potential, resting potential, L-type Ca(2+) (I(Ca)), inward rectifier potassium (I(K1)), delayed rectifier potassium (I(K)), steady-state (I(SS)), and inwardly rectifying chloride (I(Cl,ir)) currents of rat subepicardial (Epi) and subendocardial (Endo) ventricular myocytes were investigated using the patch-clamp technique. Action potential duration was shorter in Epi than in Endo cells. Acidosis (extracellular pH decreased from 7.4 to 6.5) depolarized the resting membrane potential and prolonged the time for 50% repolarization of the action potential in Epi and Endo cells, although the prolongation was larger in Endo cells. At control pH, I(Ca), I(K1), and I(SS) were not significantly different in Epi and Endo cells, but I(K) was larger in Epi cells. Acidosis did not alter I(Ca), I(K1), or I(K) but decreased I(SS); this decrease was larger in Endo cells. It is suggested that the acidosis-induced decrease in I(SS) underlies the prolongation of the action potential. I(Cl,ir) at control pH was Cd(2+) sensitive but 4,4'-disothiocyanato-stilbene-2,2'-disulfonic acid resistant. Acidosis increased I(Cl,ir); it is suggested that the acidosis-induced increase in I(Cl,ir) underlies the depolarization of the resting membrane potential.