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AJP - Cell Physiology, Vol 256, Issue 1 C147-C154, Copyright © 1989 by American Physiological Society
ARTICLES |
J. B. Smith, T. Zheng and L. Smith
Department of Pharmacology, University of Alabama, Birmingham 35294.
We examined the relationship between extracellular Na+ ([Na+]o) and cytosolic free Ca2+ ([Ca2+]i) in primary and passaged cultures of aortic muscle cells. Removing [Na+]o increased [Ca2+]i by approximately 10-fold in cells that were Na+ loaded. Decreasing [Na+]o from 140 to 32 mM caused the half-maximal increase in [Ca2+]i. [Ca2+]i exhibited a sigmoidal dependence on [Na+]o. Mg2+, a competitive inhibitor of Na2+-Ca2+ antiport in these cells, antagonized the increase in [Ca2+]i produced by lowering [Na+]o. High K+ decreased the potency of Mg2+ 6.5-fold as previously reported for Na+ gradient-dependent 45Ca2+ influx. In contrast to the Na+-loaded cells, removing [Na+]o caused no detectable change in [Ca2+]i in cells with normal Na+ even though the calculated electrochemical driving force for Na+-Ca2+ exchange was large enough to almost maximally increase [Ca2+]i in the Na+-loaded cells. We conclude that Na+-Ca2+ antiport activity is latent in the unstimulated cell at basal intracellular Na+ and Ca2+.
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