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Acidic extracellular pH-activated outwardly rectifying chloride current in mammalian cardiac myocytes

Department of Physiology, Saga University Faculty of Medicine, Saga, Japan

Submitted 9 September 2005 ; accepted in final form 2 December 2005

Extracellular acidic pH was found to induce an outwardly rectifying Cl^– current (I_Cl,acid) in mouse ventricular cells, with a half-maximal activation at pH 5.9. The current showed the permeability sequence for anions to be SCN^– > Br^– > I^– > Cl^– > F^– > aspartate, while it exhibited a time-dependent activation at large positive potentials. Similar currents were also observed in mouse atrial cells and in atrial and ventricular cells from guinea pig. Some Cl^– channel blockers (DIDS, niflumic acid, and glibenclamide) inhibited I_Cl,acid, whereas tamoxifen had little effect on it. Unlike volume-regulated Cl^– current (I_Cl,vol) and CFTR Cl^– current (I_Cl,CFTR), I_Cl,acid was independent of the presence of intracellular ATP. Activation of I_Cl,acid appeared to be also independent of intracellular Ca²⁺ and G protein. I_Cl,acid and I_Cl,vol could develop in an additive fashion in acidic hypotonic solutions. Isoprenaline-induced I_Cl,CFTR was inhibited by acidification in a pH-dependent manner in guinea pig ventricular cells. Our results support the view that I_Cl,acid and I_Cl,vol stem from two distinct populations of anion channels and that the I_Cl,acid channels are present in cardiac cells. I_Cl,acid may play a role in the control of action potential duration or cell volume under pathological conditions, such as ischemia-related cardiac acidosis.

acidosis; chloride channel; heart

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