| Autor: |
Tran, Quang-Kim, Watanabe, Hiroshi, Zhang, Xu-Xia, Takahashi, Reiko, Ohno, Ryuzo |
| Zdroj: |
Cardiovascular Research; Nov1999, Vol. 44 Issue 3, p623-631, 9p |
| Abstrakt: |
Objectives: This study was designed to investigate the involvement of myosin light-chain kinase (MLCK) in bradykinin- and thapsigargin-induced changes in intracellular Cl− and Ca2+ concentrations ([Cl−]i; [Ca2+]i) in porcine aortic endothelial cells. Methods: Using the fluorescent probes N-ethoxycarbonylmethyl-6-methoxyquinolinium bromide (MQAE) and fura-2/AM, the effects of different MLCK inhibitors on bradykinin- and thapsigargin-induced changes in [Cl−]i and [Ca2+]i were assessed. Results: Bradykinin and thapsigargin significantly decreased the MQAE fluorescence intensity, which indicates increased [Cl−]i; these changes were reversed by removal of extracellular chloride (Cl−o) and were significantly inhibited by Cl−-channel inhibitor N-phenylanthranilic acid but not by Na+–K+–Cl− cotransport inhibitor furosemide. Pretreatment with ML-9 and wortmannin, two different selective inhibitors of MLCK, significantly reduced these changes in a dose-dependent manner. The inhibitory effects of ML-9 and wortmannin on the Cl− responses were not significantly different and were not additive. Bradykinin and thapsigargin provoked large increases in [Ca2+]i, which were significantly diminished by removal of Cl−o and by pretreatment with the Cl−-channel inhibitor N-phenylanthranilic acid. Conclusions: The study shows that an increase in [Cl−]i may be involved in the Ca2+ influx in response to bradykinin and thapsigargin and that MLCK might be involved in the Cl− response. We suggest that MLCK might be involved in the Cl−-sensitive endothelial Ca2+ responses to bradykinin and thapsigargin. [ABSTRACT FROM PUBLISHER] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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