| Registro completo |
| Provedor de dados: |
Biol. Res.
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| País: |
Chile
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| Título: |
Ca2+ entry, efflux and release in smooth muscle
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| Autores: |
MATTHEW,A
SHMYGOL,A
WRAY,SUSAN
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| Data: |
2004-01-01
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| Ano: |
2004
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| Palavras-chave: |
Uterus
SR
Signalling
Ca-ATPase
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| Resumo: |
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.
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| Tipo: |
Journal article
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| Idioma: |
Inglês
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| Identificador: |
http://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0716-97602004000400017
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| Editor: |
Sociedad de Biología de Chile
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| Formato: |
text/html
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| Fonte: |
Biological Research v.37 n.4 2004
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