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 μM, 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 μM) and SKF 96365 (100 μM) completely inhibited the thapsigargin-induced [Ca2+](i) increase. The EC50 value of troglitazone (1.4 ± 0.1 μM) was lower than that of SKF 96365 (10.0 ± 3.3 μM). We suggest that troglitazone would be a useful tool to investigate the capacitative Ca2+ entry.
All Science Journal Classification (ASJC) codes