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dc.creatorMATTHEW,A
dc.creatorSHMYGOL,A
dc.creatorWRAY,SUSAN
dc.date2004-01-01
dc.date.accessioned2020-02-17T15:35:43Z
dc.date.available2020-02-17T15:35:43Z
dc.identifierhttps://scielo.conicyt.cl/scielo.php?script=sci_arttext&pid=S0716-97602004000400017
dc.identifier.urihttps://revistaschilenas.uchile.cl/handle/2250/132048
dc.descriptionControl 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.
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dc.languageen
dc.publisherSociedad de Biología de Chile
dc.relation10.4067/S0716-97602004000400017
dc.rightsinfo:eu-repo/semantics/openAccess
dc.sourceBiological Research v.37 n.4 2004
dc.subjectuterus
dc.subjectSR
dc.subjectsignalling
dc.subjectCa-ATPase
dc.titleCa2+ entry, efflux and release in smooth muscle


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