Data/hora: 04/06/2024 17:44:17

Provedor de dados: 	48	
País: 	Chile	
Título: 	Redox regulation of calcium release in skeletal and cardiac muscle	
Autores: 	HIDALGO,CECILIA; ARACENA,PAULA; SANCHEZ,GINA; DONOSO,PAULINA.	
Data: 	2002-01-01	
Ano: 	2002	
Palavras-chave: 	Redox state; Ryanodine receptors; Sarcoplasmic reticulum; Calcium release kinetics; Mg2+ inhibition; S-nitrosoglutathione.	
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+] &lt; 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	
Tipo: 	Journal article	
Idioma: 	Inglês	
Identificador: 	http://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0716-97602002000200009	
Editor: 	Sociedad de Biología de Chile	
Formato: 	text/html	
Fonte: 	Biological Research  v.35 n.2 2002