抄録
It is well known that extracellular acidosis modulates many types of ion channels in excitable and non-excitable cells. Recently, a novel Cl− current that is activated by acidic pH has been found in rat sertoli cells. In the present study, we identified a similar current (ICl.pH) in ventricular myocytes from mouse and guinea-pig. When acidic solution was applied to the cells, ICl.pH appeared with a delay of ~1 min, increased gradually, and reached a maximum in ~5 min. In contrast, the current disappeared rapidly (<1 min) upon resumption of the solution with normal pH (7.4). ICl.pH was activated in a pH-dependent manner, with a half maximal activation at about pH 6.0. ICl.pH exhibited a weak time-dependent activation, the current amplitude slightly increasing during depolarizing step pulses. I-V relationship of ICl.pH showed a strong outward rectification under symmetrical [Cl−] conditions. The anion selectivity of this current was estimated to be I− > Cl− > Asp−. Pharmacological studies showed that ICl.pH was inhibited by several Cl− channel blockers (DIDS, niflumic acid and glibenclamide). Thus, the properties of ICl.pH differ from those of other cardiac Cl− currents (volume-regulated Cl− current, inwardly rectifiying Cl− current, Ca2+-activated Cl− current or CFTR current). ICl.pH may play a role in the control of the action potential duration under pathological conditions, such as ischemia-related cardiac acidosis. [Jpn J Physiol 54 Suppl:S96 (2004)]
