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AJP - Cell Physiology, Vol 271, Issue 1 C9-34, Copyright © 1996 by American Physiological Society
ARTICLES |
A. Carl, H. K. Lee and K. M. Sanders
Department of Physiology and Cell Biology, University of Nevada School of Medicine, Reno 89557, USA.
Intracellular Ca2+ concentration ([Ca2+]i) plays a central role in regulating tone and contractility of smooth muscle cells. In contrast to the "classic" model of electromechanical coupling where membrane potential determines [Ca2+]i, it is now well established that [Ca2+]i in turn may also affect membrane potential by modulating open probabilities of ion channels. Activation by [Ca2+]i of large-conductance K+ channels, Cl- channels, and nonselective cation channels has been described, as well as block of delayed rectifier K+ channels by [Ca2+]i and [Ca2+]i-induced inactivation of Ca2+ channels. Therefore, a network consisting of positive- and negative-feedback loops regulates [Ca2+]i as well as membrane potential. In this context, we review the properties of Ca(2+)-dependent ion channels and their functional role in vascular and visceral smooth muscles. Any alteration of the "Ca2+ sensitivity" of ion channels is expected to have a profound effect on the reciprocal relationship between membrane potential and [Ca2+]i. Already several molecular factors determining Ca2+ sensitivity of Ca(2+)-activated K+ channels have been identified. We provide a working definition for Ca2+ sensitivity.
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