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Biology of Reproduction, Vol 16, 1-17, Copyright © 1977 by Society for the Study of Reproduction
1 Molecular Endocrinology Laboratory,
Veterans Administration Hospital,
Sepulveda, California and
Department of Medicine,
San Fernando Valley Medical Program,
University of California,
Los Angeles, California The complex patterns of uterine motility reflect the interaction of a number of active
compounds. Many of these agents have been shown to interact with the
-adrenergic
catecholamine-stimulable adenylate cyclase system to alter cAMP levels in the smooth muscle
layers of the uterus. From the recognized mechanism of action of cAMP, any change in the
concentration of the cyclic nucleotide should lead to change in the activity of cAMP-dependent
protein kinase and as a result a change in the activity of phosphoproteins which function at a still
more fundamental level to regulate muscle cell contractility. Treatment of the rat myometrium
with
-adrenergic agonist results in an increase in protein kinase activity associated with cellular
membranes and increased ATP-dependent Ca++-transport by these same membranes. The ability of
cAMP to duplicate the effects of
-agonist stimulation in cell free membrane preparations suggests
adrenergic control of smooth muscle cell function and hence myometrial contractility occurs by
altering the distribution of intracellular Ca++ between bound and free pools.
Note:
ACKNOWLEDGMENTS
Investigations reported here were supported by
NIH grant HD-09285 and by Research and Education
Funds from the Veterans Administration. The authors
gratefully acknowledge the technical assistance of Mr.
Abbott M. Schindler and Ms. Janet L. Swensen.
This article has been cited by other articles:
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