Receptor-coupled contractility of uterine smooth muscle: From membrane ot myofilaments

Abstract

A comprehensive understanding of the mechanisms by which agonists control uterine contraction is essential for the successful clinical management of parturition and for the timely treatment of situations involving inappropriate uterine performance. In this review we discuss some of the key stimulatory mechanisms linking receptor occupation at the myometrial plasma membrane with alteration of myofilament activation. We focus on evidence that receptor-induced membranous recruitment of the small G-protein rhoA, and its downstream effector rho-associated kinase (ROK) is crucial to agonist-induced Ca2+-sensitisation of uterine contraction and that co-ordination of this signal transduction pathway may be mediated by the actions of caveolins, proteins integral to specialised membranous regions termed caveolae.