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Am J Physiol Cell Physiol 260: C1012-C1018, 1991;
0363-6143/91 $5.00
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AJP - Cell Physiology, Vol 260, Issue 5 C1012-C1018, Copyright © 1991 by American Physiological Society


ARTICLES

Relationship between calcium current and cytosolic calcium in canine gastric smooth muscle cells

F. Vogalis, N. G. Publicover, J. R. Hume and K. M. Sanders
Department of Physiology, University of Nevada School of Medicine, Reno 89511.

We measured free intracellular Ca2+ concentration ([Ca2+]i) and Ca2+ current (ICa) simultaneously in voltage-clamped, indo-1-loaded smooth muscle cells isolated from the circular layer of the canine antrum. Resting [Ca2+]i averaged 144 +/- 20 nM in cells held at -70 mV. Depolarization positive to -50 mV elicited ICa and increased [Ca2+]i. Peak [Ca2+]i occurred between 0 and +10 mV and averaged 372 +/- 48 nM. On repolarization, [Ca2+]i decreased slowly (time constant 2-3 s) and the rate depended on the magnitude of [Ca2+]i. Cells were also voltage clamped with protocols that mimicked the upstroke and plateau phases of slow waves. With simulated plateau potentials of -55 to -45 mV, [Ca2+]i increased transiently as a result of the small transient ICa elicited by the upstroke depolarization. Sustained ICa was of sufficient magnitude with plateau depolarizations positive to -40 mV to cause a secondary rise in [Ca2+]i throughout the plateau phase. These data suggest that at the plateau potential of slow waves in situ, ICa is sufficient to cause a sustained increase in [Ca2+]i. The resulting accumulation of Ca2+ may couple the slow wave plateau to contraction and may increase the open probability of Ca(2+)-activated K channels. The latter may provide the outward current necessary to initiate repolarization.


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