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AJP - Cell Physiology, Vol 269, Issue 2 C312-C317, Copyright © 1995 by American Physiological Society
ARTICLES |
P. Meera, K. Anwer, M. Monga, C. Oberti, E. Stefani, L. Toro and B. M. Sanborn
Department of Biochemistry and Molecular Biology, University of Texas Houston Medical School, USA.
Relaxin, a hormone that is elevated during pregnancy, can suppress myometrial contractile activity. Ca(2+)-activated K+ channels (KCa) play a role in the modulation of uterine contractions and myometrial Ca2+ homeostasis and have been implicated in the control of smooth muscle excitability. We now show that relaxin stimulates KCa channels in cell-attached patches in a cell line derived from term pregnant human myometrium. This effect was prevented by the protein kinase A (PKA) antagonist, the Rp diastereomer of adenosine 3',5'-cyclic monophosphothioate (Rp-cAMPS). After patch excision, the channel was activated by PKA and inhibited by alkaline phosphatase. These data suggest that relaxin may promote myometrial quiescence in part by stimulation of KCa channels via a PKA-mediated mechanism.
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