Differential Effects of Extracellular Mg 2+ on Thrombin-Induced and Capacitative Ca 2+ Entry in Human Coronary Arterial Endothelial Cells

• Published in: Arteriosclerosis, thrombosis, and vascular biology Vol. 17; no. 11; pp. 3356 - 3361
• Main Authors: Yoshimura, Mitsuisa, Oshima, Tetsuya, Matsuura, Hideo, Inoue, Toshiaki, Kambe, Masayuki, Kajiyama, Goro
• Format: Journal Article
• Language: English
• Published: 01.11.1997
• ISSN: 1079-5642; 1524-4636
• DOI: 10.1161/01.ATV.17.11.3356

Abstract Receptor-mediated and capacitative Ca 2+ entry are the primary Ca 2+ entry pathways in endothelial cells (ECs). The mechanisms for Ca 2+ entry via these pathways have not been fully elucidated. In this study, the effect of low and high external Mg 2+ concentrations on these Ca 2+ entry pathways was examined in human coronary arterial ECs. External Mg 2+ concentration did not affect cytosolic free Mg 2+ concentration. After exposure to thrombin in Ca 2+ -free medium, addition of Ca 2+ to the medium caused a rise in cytosolic free Ca 2+ concentration ([Ca 2+ ]i), indicating thrombin-induced Ca 2+ influx. Thrombin-induced Ca 2+ influx was inhibited by not only low but also high external Mg 2+ concentrations. After depletion of endoplasmic Ca 2+ stores by thapsigargin, addition of Ca 2+ to the medium induced an increase in [Ca 2+ ]i, indicating capacitative Ca 2+ entry. Capacitative entry was found to be accelerated by low external Mg 2+ and inhibited by high external Mg 2+ concentration. Results suggest that receptor-mediated Ca 2+ influx requires external Mg 2+ but is inhibited by increased external Mg 2+ concentrations and that capacitative Ca 2+ entry is reduced by external Mg 2+ in human coronary arterial ECs.