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dc.contributor.author
Fernandez Sada, E.
dc.contributor.author
Silva Platas, C.
dc.contributor.author
Villegas, C. A.
dc.contributor.author
Rivero, S. L.
dc.contributor.author
Willis, B. C.
dc.contributor.author
García, N.
dc.contributor.author
Garza, J. R.
dc.contributor.author
Oropeza Almazán, Y.
dc.contributor.author
Valverde, Carlos Alfredo
dc.contributor.author
Mazzocchi, Gabriela
dc.contributor.author
Zazueta, C.
dc.contributor.author
Torre Amione, G.
dc.contributor.author
García Rivas, G.
dc.date.available
2017-01-26T20:18:40Z
dc.date.issued
2014-09
dc.identifier.citation
Fernandez Sada, E.; Silva Platas, C.; Villegas, C. A.; Rivero, S. L.; Willis, B. C.; et al.; Cardiac responses to β-adrenoceptor stimulation is partly dependent on mitochondrial calcium uniporter activity; Wiley; British Journal Of Pharmacology; 171; 18; 9-2014; 4207-4221
dc.identifier.issn
0007-1188
dc.identifier.uri
http://hdl.handle.net/11336/12024
dc.description.abstract
Background and Purpose: Despite the importance of mitochondrial Ca2+ to metabolic regulation and cell physiology, little is known about the mechanisms that regulate Ca2+ entry into the mitochondria. Accordingly, we established a system to determine the role of the mitochondrial Ca2+ uniporter in an isolated heart model, at baseline and during increased workload following β-adrenoceptor stimulation. Experimental Approach: Cardiac contractility, oxygen consumption and intracellular Ca2+ transients were measured in ex vivo perfused murine hearts. Ru360 and spermine were used to modify mitochondrial Ca2+ uniporter activity. Changes in mitochondrial Ca2+ content and energetic phosphate metabolite levels were determined. Key Results: The addition of Ru360, a selective inhibitor of the mitochondrial Ca2+ uniporter, induced progressively and sustained negative inotropic effects that were dose-dependent with an EC50 of 7 μM. Treatment with spermine, a uniporter agonist, showed a positive inotropic effect that was blocked by Ru360. Inotropic stimulation with isoprenaline elevated oxygen consumption (2.7-fold), Ca2+-dependent activation of pyruvate dehydrogenase (5-fold) and mitochondrial Ca2+ content (2.5-fold). However, in Ru360-treated hearts, this parameter was attenuated. In addition, β-adrenoceptor stimulation in the presence of Ru360 did not affect intracellular Ca2+ handling, PKA or Ca2+/calmodulin-dependent PK signalling. Conclusions and Implications: Inhibition of the mitochondrial Ca2+ uniporter decreases β-adrenoceptor response, uncoupling between workload and production of energetic metabolites. Our results support the hypothesis that the coupling of workload and energy supply is partly dependent on mitochondrial Ca2+ uniporter activity.
dc.format
application/pdf
dc.language.iso
eng
dc.publisher
Wiley
dc.rights
info:eu-repo/semantics/restrictedAccess
dc.rights.uri
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.subject
Mitochondria
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Biochemical Pharmacology
dc.subject
Catecholamines
dc.subject
Ion Channles
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Otras Medicina Básica
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Medicina Básica
dc.subject.classification
CIENCIAS MÉDICAS Y DE LA SALUD
dc.title
Cardiac responses to β-adrenoceptor stimulation is partly dependent on mitochondrial calcium uniporter activity
dc.type
info:eu-repo/semantics/article
dc.type
info:ar-repo/semantics/artículo
dc.type
info:eu-repo/semantics/publishedVersion
dc.date.updated
2017-01-25T13:57:50Z
dc.identifier.eissn
1476-5381
dc.journal.volume
171
dc.journal.number
18
dc.journal.pagination
4207-4221
dc.journal.pais
Estados Unidos
dc.journal.ciudad
Hoboken
dc.description.fil
Fil: Fernandez Sada, E.. Tecnológico de Monterrey; México
dc.description.fil
Fil: Silva Platas, C.. Tecnológico de Monterrey; México
dc.description.fil
Fil: Villegas, C. A.. Tecnológico de Monterrey; México
dc.description.fil
Fil: Rivero, S. L.. Tecnológico de Monterrey; México
dc.description.fil
Fil: Willis, B. C.. Tecnológico de Monterrey; México
dc.description.fil
Fil: García, N.. Tecnológico de Monterrey; México. Instituto de Cardiología y Medicina Vascular; México
dc.description.fil
Fil: Garza, J. R.. Tecnológico de Monterrey; México
dc.description.fil
Fil: Oropeza Almazán, Y.. Tecnológico de Monterrey; México
dc.description.fil
Fil: Valverde, Carlos Alfredo. Consejo Nacional de Investigaciones Cientificas y Tecnicas. Centro Cientifico Tecnológico la Plata. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani"; Argentina. Universidad Nacional de la Plata. Facultad de Ciencias Médicas; Argentina
dc.description.fil
Fil: Mazzocchi, Gabriela. Consejo Nacional de Investigaciones Cientificas y Tecnicas. Centro Cientifico Tecnológico la Plata. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani"; Argentina. Universidad Nacional de la Plata. Facultad de Ciencias Médicas; Argentina
dc.description.fil
Fil: Zazueta, C.. Instituto Nacional de Cardiología ‘Ignacio Chávez’; México
dc.description.fil
Fil: Torre Amione, G.. Tecnológico de Monterrey; México. Instituto de Cardiología y Medicina Vascular; México
dc.description.fil
Fil: García Rivas, G.. Tecnológico de Monterrey; México. Instituto de Cardiología y Medicina Vascular; México
dc.journal.title
British Journal Of Pharmacology
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/doi/http://dx.doi.org/10.1111/bph.12684
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/http://onlinelibrary.wiley.com/doi/10.1111/bph.12684/abstract


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