| Registro completo |
| Provedor de dados: |
Biol. Res.
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| País: |
Chile
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| Título: |
Redox regulation of calcium release in skeletal and cardiac muscle
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| Autores: |
HIDALGO,CECILIA
ARACENA,PAULA
SANCHEZ,GINA
DONOSO,PAULINA
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| Data: |
2002-01-01
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| Ano: |
2002
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| Palavras-chave: |
Redox state
Ryanodine receptors
Sarcoplasmic reticulum
Calcium release kinetics
Mg2+ inhibition
S-nitrosoglutathione
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| Resumo: |
In skeletal and cardiac muscle cells, specific isoforms of the Ryanodine receptor channels mediate Ca2+ release from the sarcoplasmic reticulum. These channels are highly susceptible to redox modifications, which regulate channel activity. In this work, we studied the effects of Ca2+ (endogenous agonist) and Mg2+ (endogenous inhibitor) on the kinetics of Ca2+ release from sarcoplasmic reticulum vesicles isolated from skeletal or cardiac mammalian muscle. Native skeletal vesicles exhibited maximal stimulation of release kinetics by 10-20 µM [Ca2+], whereas in native cardiac vesicles, maximal stimulation of release required only 1 µM [Ca2+]. In 10 µM [Ca2+], free [Mg2+] < 0.1 mM produced marked inhibition of release from skeletal vesicles but free [Mg2+] 0.8 mM did not affect release from cardiac vesicles. Incubation of skeletal or cardiac vesicles with the oxidant thimerosal increased their susceptibility to stimulation by Ca2+ and decreased the inhibitory effect of Mg2+ in skeletal vesicles. Sulfhydryl-reducing agents fully reversed the effects of thimerosal. The endogenous redox species, glutathione disulfide and S-nitrosoglutathione, also stimulated release from skeletal sarcoplasmic reticulum vesicles. In 10 µM [Ca2+], 35S-nitrosoglutathione labeled a protein fraction enriched in release channels through S-glutathiolation. Free [Mg2+] 1 mM or decreasing free [Ca2+] to the nM range prevented this reaction. Possible physiological and pathological consequences of redox modification of release channels on Ca2+ signaling in heart and muscle cells are discussed
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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=S0716-97602002000200009
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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.35 n.2 2002
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