Fast Na+ Current and Ca2+ Currents in Smooth Muscles
Most smooth muscle (SM) cells normally do not possess fast Na+ channels, and inward current for the action potential (AP) is carried primarily through slow (L-type) Ca2+ channels. The slow Ca2+ channel activity is regulated by several mechanisms, as is well known for myocardial cells. In myocardial cells, cyclic AMP and cAMP-dependent protein kinase (cA-PK) stimulate slow Ca2+ channel activity, whereas cyclic GMP and cGMP-dependent protein kinase (cG-PK) inhibit channel activity (reviewed in Sperelakis et al., 1992). Phosphorylation by PK-C also stimulates activity of the myocardial slow Ca2+ channels (Domenici & Rogers, 1988). Intracellular ATP also modulates slow Ca2+ channel activity in myocardial cells, ATP being obligatory for channel activity (Sperelakis & Schneider, 1976; O’Rourke et al., 1992). Acidosis rapidly, reversibly, and rather selectively inhibits the slow Ca2+ channels in cardiac muscle (Vogel & Sperelakis, 1977; Belardinelli et al., 1979; Irisawa and Sato, 1987). Gating of myocardial Ca2+ slow channels by Gs-protein (GTP-activated alpha subunit) has also been demonstrated (Yatani et al., 1988). Intracellular ATP also modulates activity of slow Ca2+ channels in SM cells (Ohya and Sperelakis, 1989a, b), and phosphorylation by either cAMP or cGMP-mediated pathways inhibit slow Ca2+ channel activity (Bkaily et al., 1988a).
KeywordsCardiol EGTA Diltiazem Pertussis Cali
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