AJP - Cell Physiology, Vol 263, Issue 1 C30-C38, Copyright © 1992 by American Physiological Society
Heat shock increases cytosolic free Ca2+ concentration via Na(+)-Ca2+ exchange in human epidermoid A 431 cells
J. G. Kiang, M. L. Koenig and R. C. Smallridge
Department of Clinical Physiology, Walter Reed Army Institute of Research, Washington, DC 20307-5100.
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 degrees C was 87 +/- 5 nM (n = 105). When
cells were subjected to hyperthermia (40-50 degrees C), [Ca2+]i increased
in a temperature- and time-dependent manner. The maximal increase in cells
exposed to 45 degrees 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
microM, 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 microM) and
5'-(N,N-dimethyl)-amiloride (1 microM). These results suggest heat
activates the Na(+)-Ca2+ exchange system so as to increase [Ca2+]i and
reduce [Na+]i.
