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Receptor‐Coupled Contractility of Uterine Smooth Muscle: From Membrane to Myofilaments
Author(s) -
Lee Y.H.,
Hwang M.K.,
Morgan K. G.,
Taggart Michael J.
Publication year - 2001
Publication title -
experimental physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.925
H-Index - 101
eISSN - 1469-445X
pISSN - 0958-0670
DOI - 10.1113/eph8602184
Subject(s) - rhoa , caveolae , receptor , contractility , myofilament , microbiology and biotechnology , signal transduction , g protein coupled receptor , contraction (grammar) , endocrinology , muscle contraction , myometrium , agonist , biology , g protein , medicine , chemistry , uterus , myocyte
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 Ca 2+ ‐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.