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vol.37 issue4Peptide and protein modulation of local Ca2+ release events in permeabilized skeletal muscle fibersPossible link of different slow calcium signals generated by membrane potential and hormones to differential gene expression in cultured muscle cells author indexsubject indexarticles search
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Biological Research

Print version ISSN 0716-9760

Abstract

MATTHEW, A; SHMYGOL, A  and  WRAY, SUSAN. Ca2+ entry, efflux and release in smooth muscle. Biol. Res. [online]. 2004, vol.37, n.4, pp.617-624. ISSN 0716-9760.  http://dx.doi.org/10.4067/S0716-97602004000400017.

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.

Keywords : uterus; SR; signalling; Ca-ATPase.

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