This review summarizes the biophysical and pharmacological properties of Ca(2+)-activated Cl- channels in smooth muscle, suggesting their role in membrane depolarization and contraction.
In this review we discuss the properties of the Ca(2+)-activated Cl- current ICl(Ca) recorded in isolated smooth muscle cells with electrophysiological techniques and speculate on the possible physiological role(s) of ICl(Ca) in smooth muscle function. In particular, we concentrate on 1) the Ca2+ dependence of ICl(Ca), 2) the mechanisms that link pharmacological receptor stimulation on the cell surface membrane to activation of ICl(Ca), 3) the biophysical properties of ICl(Ca), and 4) the pharmacology of ICl(Ca). It is evident that a diverse array of pharmacological agonists can evoke ICl(Ca) in many types of smooth muscle, and it seems that the well-established G protein-phosphoinositide metabolism (inositol 1,4,5-trisphosphate)-intracellular Ca2+ store pathway couples the receptor to the membrane channels. Also, the results indicate that the biophysical and pharmacological properties of ICl(Ca) are not only similar in the various smooth muscle types studied so far but, possibly, are also similar to ICl(Ca) in non-smooth muscle tissue. Evidence is presented that the Ca(2+)-activated Cl- channel exists in two states, open and closed, with a relatively long mean open time and that some of the agents that inhibit ICl(Ca) interact directly with the open channel. It is suggested that the most likely role of ICl(Ca) in smooth muscle is to produce membrane depolarization and contraction to neurotransmitters and local mediators.
Large et al. (Thu,) studied this question.
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