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AJP - Cell Physiology, Vol 260, Issue 5 C1012-C1018, Copyright © 1991 by American Physiological Society
ARTICLES |
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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