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Mitochondrial K+ transport and cardiac protection during ischemia/reperfusion
Carreira, R. S; Facundo, H. T. F; Kowaltowski, A. J.
Afiliación
  • Carreira, R. S; Universidade de São Paulo. Instituto de Química. Departamento de Bioquímica. São Paulo. BR
  • Facundo, H. T. F; Universidade de São Paulo. Instituto de Química. Departamento de Bioquímica. São Paulo. BR
  • Kowaltowski, A. J; Universidade de São Paulo. Instituto de Química. Departamento de Bioquímica. São Paulo. BR
Rev. bras. pesqui. méd. biol ; Braz. j. med. biol. res;38(3): 345-352, mar. 2005. ilus
Article en En | LILACS | ID: lil-394809
Biblioteca responsable: BR1.1
RESUMO
Mitochondrial ion transport, oxidative phosphorylation, redox balance, and physical integrity are key factors in tissue survival following potentially damaging conditions such as ischemia/reperfusion. Recent research has demonstrated that pharmacologically activated inner mitochondrial membrane ATP-sensitive K+ channels (mitoK ATP) are strongly cardioprotective under these conditions. Furthermore, mitoK ATP are physiologically activated during ischemic preconditioning, a procedure which protects against ischemic damage. In this review, we discuss mechanisms by which mitoK ATP may be activated during preconditioning and the mitochondrial and cellular consequences of this activation, focusing on end-effects which may promote ischemic protection. These effects include decreased loss of tissue ATP through reverse activity of ATP synthase due to increased mitochondrial matrix volumes and lower transport of adenine nucleotides into the matrix. MitoK ATP also decreases the release of mitochondrial reactive oxygen species by promoting mild uncoupling in concert with K+/H+ exchange. Finally, mitoK ATP activity may inhibit mitochondrial Ca2+ uptake during ischemia, which, together with decreased reactive oxygen release, can prevent mitochondrial permeability transition, loss of organelle function, and loss of physical integrity. We discuss how mitochondrial redox status, K+ transport, Ca2+ transport, and permeability transitions are interrelated during ischemia/reperfusion and are determinant factors regarding the extent of tissue damage.
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Texto completo: 1 Colección: 01-internacional Base de datos: LILACS Asunto principal: Daño por Reperfusión Miocárdica / Canales de Potasio / Mitocondrias Cardíacas Límite: Humans Idioma: En Revista: Braz. j. med. biol. res / Rev. bras. pesqui. méd. biol Asunto de la revista: BIOLOGIA / MEDICINA Año: 2005 Tipo del documento: Article / Project document País de afiliación: Brasil Pais de publicación: Brasil
Texto completo
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Imprimir
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Texto completo: 1 Colección: 01-internacional Base de datos: LILACS Asunto principal: Daño por Reperfusión Miocárdica / Canales de Potasio / Mitocondrias Cardíacas Límite: Humans Idioma: En Revista: Braz. j. med. biol. res / Rev. bras. pesqui. méd. biol Asunto de la revista: BIOLOGIA / MEDICINA Año: 2005 Tipo del documento: Article / Project document País de afiliación: Brasil Pais de publicación: Brasil