Relaxin stimulates myometrial calcium-activated potassium channel
activity via protein kinase a.
Meera, P., K. Anwer, M. Monga, C. Oberti, E. Stefani, L. Toro, and B.
M. Sanborn.
Department of Biochemistry and Molecular Biology and Department of
Obstetrics, Gynecology, Reproductive Sciences, University of Texas
Houston Medical School, Houston TX 77030; Department of Molecular
Physiology and Biophysics, Baylor College of Medicine, Houston TX
77030
APStracts 2:0126C, 1995.
Relaxin, a hormone that is elevated during pregnancy, can suppress
myometrial contractile activity. Calcium-activated K+ channels (KCa)
play a role in the modulation of uterine contractions and myometrial
calcium 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 Rp-cAMP[S]. Following 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.
Received 21 December 1994; accepted in final form 13 January
1995.
APS Manuscript Number C733-4.
Article publication pending Am. J. Physiol. (Cell Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 10 March 1995.