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Biol. Res ; 37(4): 617-624, 2004. graf
Article in English | LILACS | ID: lil-437517

ABSTRACT

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 percet and 70 percet 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.


Subject(s)
Rats , Animals , Female , /physiology , /metabolism , Calcium/metabolism , Uterine Contraction/physiology , Uterine Contraction/metabolism , Myometrium/physiology , Myometrium/metabolism , Sarcoplasmic Reticulum/physiology , Sarcoplasmic Reticulum/metabolism , Calcium Channels, L-Type/metabolism , Calcium Channels/metabolism , Muscle, Smooth/physiology
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