This study characterized cytosolic free Ca2+ concentration ([Ca2+](i)) in normal and thermally injured human epidermoid A 431 cells. The resting [Ca2+](i) in normal cells at 37°C was 87 ± 5 nM (n = 105). When cells were subjected to hyperthermia (40-50°C), [Ca2+](i) increased in a temperature- and time-dependent manner. The maximal increase in cells exposed to 45°C was observed at 20 min; [Ca2+](i) returned to normal within 1 h. The heat-induced [Ca2+](i) increase depended on the presence of external Ca2+, La3+ and Cd2+ but not Co2+, verapamil, or nifedipine attenuated the heat-induced [Ca2+](i) increase. TMB-8 partially blocked the increase in [Ca2+](i) but pertussis toxin and cholera toxin pretreatment did not. The magnitude of the heat-induced [Ca2+](i) increase or 45Ca2+ uptake depended on the presence of extracellular Na+. Heat treatment reduced the apparent Michaelis constant for external Ca2+ from 490 ± 91 to 210 ± 60 μM, whereas the maximal velocity remained the same. The intracellular Na+ concentration decreased 62.5% after heating. The heat-induced [Ca2+](i) increase was completely blocked by amiloride (5 μM) and 5'-(N,N-dimethyl)- amiloride (1 μM). These results suggest heat activates the Na+-Ca2+ exchange system so as to increase [Ca2+](i) and reduce [Na+](i).
|Original language||English (US)|
|Journal||American Journal of Physiology - Cell Physiology|
|Issue number||1 32-1|
|State||Published - 1992|
- sodium-calcium exchanger
ASJC Scopus subject areas
- Cell Biology