Repository logo
 
Publication

Vantagens Na Utilização do Carvedilol Em Relação Ao Propranolol Na Protecção da Função Mitocondrial Cardíaca

2004Journal article Open access
Simple item page
dc.contributor.authorOliveira, PJ
dc.contributor.authorRolo, AP
dc.contributor.authorSardão, VA
dc.contributor.authorMonteiro, P
dc.contributor.authorGonçalves, L
dc.contributor.authorProvidência, LA
dc.contributor.authorPalmeira, CM
dc.contributor.authorMoreno, AJ
dc.date.accessioned2008-12-12T14:59:02Z
dc.date.available2008-12-12T14:59:02Z
dc.date.issued2004
dc.description.abstractBACKGROUND: Carvedilol is a neurohormonal antagonist of multiple action which is used in clinical practice for the treatment of congestive heart failure, mild to moderate hypertension and myocardial infarction. Previous results from our group have demonstrated that one of the main targets for the protective effect of carvedilol is the cardiac mitochondrial network. In-this work, we compare the effect of carvedilol with propranolol in different models of mitochondrial dysfunction and in the generation of transmembrane electric potential (EP). We further tested if carvedilol was able to inhibit the mitochondrial permeability transition (MPT) induced by doxorubicin and calcium-dependent cytochrome c release, a phenomenon frequently associated with apoptotic cell death. METHODS: Cardiac mitochondria were isolated by differential centrifugation. Oxygen consumption and mitochondrial EP were determined using an oxygen electrode and a tetraphenylphosphonium-sensitive electrode, respectively. Changes in mitochondrial volume and the release of cytochrome c were measured with spectrophotometric techniques. RESULTS: Propranolol, compared with carvedilol, had only a marginal effect, not only in protection against MPT induction, but also against oxygen consumption linked to the oxidation of external NADH, a process that is considered by several authors as key in the cardiotoxicity of doxorubicin. Regarding EP generation, propranolol had no effect, in contrast to carvedilol, which was confirmed to act as a protonophore. For the first time we also show that carvedilol inhibits the MPT induced by doxorubicin and calcium-dependent cytochrome c release. CONCLUSIONS: With this work, we further support the notion that carvedilol is effective in several models of mitochondrial dysfunction, particularly those involving oxidative stress. The results demonstrate that for some pathological conditions, carvedilol and propranolol have different mechanisms of action at the sub-cellular level, as propranolol seems to lack effectiveness in the protection of cardiac mitochondria.en
dc.identifier.citationRev Port Cardiol. 2004 Oct;23(10):1291-8en
dc.identifier.urihttp://hdl.handle.net/10400.4/338
dc.language.isoporen
dc.publisherSociedade Portuguesa de Cardiologiaen
dc.subjectMitocôndrias Cardiacasen
dc.subjectPropranololen
dc.titleVantagens Na Utilização do Carvedilol Em Relação Ao Propranolol Na Protecção da Função Mitocondrial Cardíacaen
dc.title.alternativeAdvantages in the use of carvedilol versus propranolol for the protection of cardiac mitochondrial functionen
dc.typejournal article
dspace.entity.typePublication
rcaap.rightsopenAccess
rcaap.typearticleen

Files

Original bundle
Now showing 1 - 1 of 1
Thumbnail Image
Name:
Vantagens Na Utilização do Carvedilol Em Relação Ao Propranolol Na Protecção da Função Mitocondrial Cardíaca.pdf
Size:
200.04 KB
Format:
Adobe Portable Document Format
Download
License bundle
Now showing 1 - 1 of 1
No Thumbnail Available
Name:
license.txt
Size:
1.8 KB
Format:
Item-specific license agreed upon to submission
Description:
Download

Collections

CAR - Artigos