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Am J Physiol Heart Circ Physiol 283: H412-H422, 2002. First published March 28, 2002; doi:10.1152/ajpheart.01042.2001
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Vol. 283, Issue 1, H412-H422, July 2002

Electrophysiological response of rat ventricular myocytes to acidosis

Kimiaki Komukai, Fabien Brette, Caroline Pascarel, and Clive H. Orchard

School of Biomedical Sciences, University of Leeds, Leeds LS2 9NL, United Kingdom

The effects of acidosis on the action potential, resting potential, L-type Ca2+ (ICa), inward rectifier potassium (IK1), delayed rectifier potassium (IK), steady-state (ISS), and inwardly rectifying chloride (ICl,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, ICa, IK1, and ISS were not significantly different in Epi and Endo cells, but IK was larger in Epi cells. Acidosis did not alter ICa, IK1, or IK but decreased ISS; this decrease was larger in Endo cells. It is suggested that the acidosis-induced decrease in ISS underlies the prolongation of the action potential. ICl,ir at control pH was Cd2+ sensitive but 4,4'-disothiocyanato-stilbene-2,2'-disulfonic acid resistant. Acidosis increased ICl,ir; it is suggested that the acidosis-induced increase in ICl,ir underlies the depolarization of the resting membrane potential.

action potential; chloride current; potassium current; perforated patch


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