The Role of Cyclic AMP in the Regulation of Smooth Muscle Cell Contraction in the Uterus

Abstract

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 β-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 β-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 β-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.