作者: Andre Kamkin , Irina Kiseleva , Gerrit Isenberg
DOI: 10.1007/S00424-003-1018-Y
关键词:
摘要: Stretch-activated non-selective cation currents (I SAC) constitute a mechanism that can induce cardiac arrhythmias. We studied I SAC in mouse ventricular myocytes by stretching part of the cell surface between patch-pipette and motor-driven glass stylus. In non-clamped cells, local stretch depolarised induced after-depolarisations extrasystoles. voltage-clamped cells (K+ suppressed) activated had nearly linear voltage dependence reversed polarity −12 0 mV. Conductance G increased with extent stretch. was not Cl− current (insensitivity to replacement aspartate−). Ca2+-activated 5 mM intracellular BAPTA). blocked µM GdCl3 or 75 extracellular (e.c.) CaCl2. Removal e.c. CaCl2 2.5-fold, as if were sensitive Ca2+ Gd3+. Replacement 150 Na+ Cs+, Li+, tetraethylammonium (TEA+) N-methyl d-glucosamine (NMDG+) yielded suggested for conductance selectivity Cs>G Na>G Li>G TEA>G NMDG. suppressed cytochalasin D, an intact F-actin cytoskeleton necessary activation SAC.