Characteristic of Cl− current induced by ATP in bovine aortic endothelial cells

✍ Scribed by Wen-Li Wei; Hua He; Yong-Yuan Guan

• Publisher: John Wiley and Sons
• Year: 2003
• Tongue: English
• Weight: 80 KB
• Volume: 58
• Category: Article
• ISSN: 0272-4391
• DOI: 10.1002/ddr.10129

✦ Synopsis

Abstract

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.