Troglitazone inhibits the capacitative Ca2+ entry in endothelial cells

To investigate the effects of troglitazone on the capacitative Ca2+ entry, we monitored changes in cytosolic Ca2+ concentrations ([Ca2+]i) induced by thapsigargin in fura-2-loaded porcine endothelial cells in situ and in primary culture. In aortic valve endothelial cells in situ, thapsigargin induced sustained elevation of [Ca2+]i. Both troglitazone and SKF 96365 inhibited the steady state increase in [Ca2+]i in a concentration-dependent manner. At 30 microM, troglitazone and SKF 96365 inhibited the [Ca2+]i elevation to 19.4 +/- 3.6% and 43.9 +/- 4.5%, respectively. In aortic endothelial cells in primary culture, both troglitazone (10 microM) and SKF 96365 (100 microM) completely inhibited the thapsigargin-induced [Ca2+]i increase. The EC50 value of troglitazone (1.4 +/- 0.1 microM) was lower than that of SKF 96365 (10.0 +/- 3.3 microM). We suggest that troglitazone would be a useful tool to investigate the capacitative Ca2+ entry.