抄録
The properties of VSOR Cl− currents in single ventricular myocytes isolated from ClC-3 knockout mice were compared with those from ClC-3-expressing wild-type or heterozygous mice. Basal whole-cell currents recorded under isotonic conditions were indistinguishable between ClC-3-deficient and -expressing cells. ClC-3-deficient cardiomyocytes responded to osmotic swelling with activation of whole-cell anion currents that exhibited moderate outward rectification, time- and voltage-dependent inactivation, low-field anion selectivity and sensitivity to a Cl− channel blocker. These biophysical and pharmacological properties of VSOR Cl− currents in ClC-3-deficient cells were identical to those in ClC-3-expressing cells. Moreover, the VSOR Cl− current density, which is an indicator of plasmalemmal expression of the functional channels, was essentially the same in cells isolated from these 3 types of mice. Activation of protein kinase C (PKC) was found to upregulate VSOR Cl− currents in ClC-3-deficient and -expressing cells. This PKC effect is opposite to the reported downregulating effect of PKC activators on ClC-3-associated Cl− currents. Thus, it is concluded that functional expression of VSOR Cl− channels on the plasma membrane in mouse cardiomyocytes is independent of molecular expression of ClC-3. [Jpn J Physiol 54 Suppl:S68 (2004)]
