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AJP - Lung Cellular and Molecular Physiology, Vol 264, Issue 3 323-L328, Copyright © 1993 by American Physiological Society
ARTICLES |
C. G. Salvaterra and W. F. Goldman
Department of Medicine, Baltimore Veterans Affairs Hospital, Maryland.
The effects of hypoxia on the cytosolic Ca2+ concentration, [Ca2+]i, were characterized in cultured pulmonary arterial smooth muscle (PASM) cells. Reducing O2 tension (PO2) from 150 to < 25 Torr induced a reversible 100-200% increase in [Ca2+]i that was characterized by two components: an early rise in [Ca2+]i that was dependent on the rate, as well as the magnitude, of decline in PO2 and a later, steady-state increase that was independent of the rate at which PO2 changed. Caffeine lowered [Ca2+]i during normoxia and blocked the early component of the response to hypoxia, whereas the steady-state hypoxic response was only partially inhibited. Like hypoxia, thapsigargin (TG) elevated [Ca2+]i, and there was no additional hypoxia-induced elevation in [Ca2+]i at any time after exposure to TG. At steady state, the hypoxic responses were completely reversed by removal of extracellular Ca2+, whereas, on average, verapamil and nifedipine attenuated the hypoxia-induced increases in [Ca2+]i by only 44 and 35%, respectively. These results suggest that hypoxia-induced elevation of [Ca2+]i in PASM cells consists of an early release of Ca2+ from the sarcoplasmic reticulum and a later influx of extracellular Ca2+, in part, through nifedipine- and verapamil-insensitive Ca2+ channels. The results are consistent with the idea that hypoxia and thapsigargin may share common mechanisms for tonically increasing [Ca2+]i.
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