Open AccessCa2+ entry, efflux and release in smooth muscle
Author(s) -
A Matthew,
Anatoly Shmygol,
Susan Wray
Publication year - 2004
Publication title -
biological research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.127
H-Index - 55
eISSN - 0717-6287
pISSN - 0716-9760
DOI - 10.4067/s0716-97602004000400017
Subject(s) - endoplasmic reticulum , biophysics , contraction (grammar) , calmodulin , efflux , myometrium , intracellular , myosin , microbiology and biotechnology , plasma membrane ca2+ atpase , chemistry , sodium calcium exchanger , muscle contraction , myosin light chain kinase , biology , atpase , medicine , endocrinology , biochemistry , enzyme , uterus
Control of smooth muscle is vital for health. The major route to contraction is a rise in intracellular [Ca2+], determined by the entry and efflux of Ca2+ and release and re-uptake into the sarcoplasmic reticulum (SR). We review these processes in myometrium, to better understand excitation-contraction coupling and develop strategies for preventing problematic labours. The main mechanism of elevating [Ca2+] is voltage-gated L-type channels, due to pacemaker activity, which can be modulated by agonists. The rise of [Ca2+] produces Ca-calmodulin and activates MLCK. This phosphorylates myosin and force results. Without Ca2+ entry uterine contraction fails. The Na/Ca exchanger (NCX) and plasma membrane Ca-ATPase (PMCA) remove Ca2+, with contributions of 30% and 70% respectively. Studies with PMCA-4 knockout mice show that it contributes to reducing [Ca2+] and relaxation. The SR contributes to relaxation by vectorially releasing Ca2+ to the efflux pathways, and thereby increasing their rates. Agonists binding produces IP3 which can release Ca from the SR but inhibition of SR Ca2+ release increases contractions and Ca2+ transients. It is suggested that SR Ca2+ targets K+ channels on the surface membrane and thereby feedback to inhibit excitability and contraction.