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Characteristic of Cl − current induced by ATP in bovine aortic endothelial cells
Author(s) -
Wei WenLi,
He Hua,
Guan YongYuan
Publication year - 2003
Publication title -
drug development research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.582
H-Index - 60
eISSN - 1098-2299
pISSN - 0272-4391
DOI - 10.1002/ddr.10129
Subject(s) - dids , glibenclamide , chemistry , biophysics , channel blocker , patch clamp , reversal potential , furosemide , ion transporter , membrane potential , endothelial stem cell , endocrinology , medicine , biochemistry , calcium , biology , membrane , receptor , in vitro , organic chemistry , diabetes mellitus
Patch‐clamp whole‐cell recording techniques were used to study ATP‐induced Cl ‐ current and the effects of Cl ‐ channel blockers on NO release in bovine aortic endothelial cells. ATP evoked an outward rectified Cl ‐ current with a reversal potential of −29±3 mV. This outward rectified Cl ‐ current was dependent on Ca 2+ influx, but not Ca 2+ release. In Ca 2+ ‐free medium, ATP did not produce the Cl ‐ current; however, subsequent addition of Ca 2+ to the medium evoked an ATP‐induced outward rectified Cl ‐ current. Furosemide, glibenclamide, and DIDS inhibited ATP‐activated Cl ‐ current in a concentration‐dependent manner with maximal inhibition of 88±4%, 93±1%, and 79±3%, respectively. The IC 50 values of furosemide, glibenclamide, and DIDS were 6.2±2.6, 29.6±12.3, and 21.0±13.4 µM, respectively. These effects of Cl ‐ channel blockers matched those on NO release from endothelial cells. Our data suggest that ATP‐induced Ca 2+ entry followed by increased [Ca 2+ ] i activates Ca 2+ ‐activated Cl ‐ channels which mediate NO release from endothelial cells. Drug Dev. Res. 58:53–56, 2003. © 2003 Wiley‐Liss, Inc.