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AJP - Cell Physiology, Vol 266, Issue 5 C1459-C1463, Copyright © 1994 by American Physiological Society
ARTICLES |
G. Perez and L. Toro
Department of Molecular Physiology and Biophysics, Baylor College of Medicine, Houston 77030.
Uterine excitability depends on ion channel activity, the expression of which is regulated by sexual hormones. We show now that the action of protein kinase A (PKA) on large-conductance calcium-activated K+ (KCa) channel activity also depends on the hormonal status. PKA-dependent phosphorylation of reconstituted KCa channels from midpregnant rats usually stimulated channel activity; in contrast, KCa channels from nonpregnant rat and human myometrium were primarily inhibited by this mechanism. Both effects were reversible by phosphatase treatment. These results suggest that one important factor modulating uterine contractility during pregnancy or the regular cycle may be the differential response of KCa channels toward PKA-induced phosphorylation.
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