NHE-1 and NHE-6 Activities : Ischemic and Reperfusion Injury

The study published in this issue of <i>Circulation Research</i> showing that a null mutation of NHE-1 improves the tolerance of the heart to ischemia and reperfusion (I/R) is an important contribution for the following reasons: (1) In the animals with null mutation, contracture during t...

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Autores principales: Cingolani, Horacio Eugenio, Ennis, Irene Lucía, Mosca, Susana María
Formato: Articulo
Lenguaje:Inglés
Publicado: 2003
Materias:
Ciencias Médicas
Apoptosis
Myocardial infarction
Necrosis
NHE-1
NHE-6
Acceso en línea:http://sedici.unlp.edu.ar/handle/10915/84540
Aporte de:
SEDICI (UNLP) de Universidad Nacional de La Plata
id I19-R120-10915-84540
record_format dspace
institution Universidad Nacional de La Plata
institution_str I-19
repository_str R-120
collection SEDICI (UNLP)
language Inglés
topic Ciencias Médicas
Apoptosis
Myocardial infarction
Necrosis
NHE-1
NHE-6
spellingShingle Ciencias Médicas
Apoptosis
Myocardial infarction
Necrosis
NHE-1
NHE-6
Cingolani, Horacio Eugenio
Ennis, Irene Lucía
Mosca, Susana María
NHE-1 and NHE-6 Activities : Ischemic and Reperfusion Injury
topic_facet Ciencias Médicas
Apoptosis
Myocardial infarction
Necrosis
NHE-1
NHE-6
description The study published in this issue of <i>Circulation Research</i> showing that a null mutation of NHE-1 improves the tolerance of the heart to ischemia and reperfusion (I/R) is an important contribution for the following reasons: (1) In the animals with null mutation, contracture during the ischemic period was less and ATP levels were preserved compared with wild-type animals. This observation, on the one hand, provides evidence that protection by downregulation of NHE-1 during the ischemic period itself is indeed possible and, on the other hand, it argues against the suggestion that the exchanger is inactive during this same period. (2) In contrast with chronic blockade of the NHE-1 by pharmacological interventions, the long-term absence of the exchanger does not elicit major compensatory changes that, in turn, might negate the cardioprotective effect of blocking its activity for a relative short term. This point is related to a recent publication showing that long-term treatment with the NHE-1 blocker cariporide is followed by an upregulation of the functional units of the exchanger in a similar way to the well-known tolerance phenomenon following β-adrenergic receptor blockade. The absence of such upregulation negates possible hypersensitivity to ischemia upon withdrawal of the medication. The risk is evident in hearts with upregulation of NHE-1, which gain Na<SUP>+</SUP><SUB>i</SUB> more rapidly during ischemia, and show impaired recovery after reperfusion. (3) No additional protection was obtained by adding the NHE-1 blocker eniporide to the NHE-1 null mice, suggesting that there is not another NHE isoform that can be blocked with this compound to add additional protection; the findings additionally hint that the attenuation of the injury obtained by the absence of the sarcolemmal NHE-1 is maximal and, therefore, no further beneficial effect will be detected by blocking the mitochondrial NHE (MNHE).
format Articulo
Articulo
author Cingolani, Horacio Eugenio
Ennis, Irene Lucía
Mosca, Susana María
author_facet Cingolani, Horacio Eugenio
Ennis, Irene Lucía
Mosca, Susana María
author_sort Cingolani, Horacio Eugenio
title NHE-1 and NHE-6 Activities : Ischemic and Reperfusion Injury
title_short NHE-1 and NHE-6 Activities : Ischemic and Reperfusion Injury
title_full NHE-1 and NHE-6 Activities : Ischemic and Reperfusion Injury
title_fullStr NHE-1 and NHE-6 Activities : Ischemic and Reperfusion Injury
title_full_unstemmed NHE-1 and NHE-6 Activities : Ischemic and Reperfusion Injury
title_sort nhe-1 and nhe-6 activities : ischemic and reperfusion injury
publishDate 2003
url http://sedici.unlp.edu.ar/handle/10915/84540
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AT ennisirenelucia nhe1andnhe6activitiesischemicandreperfusioninjury
AT moscasusanamaria nhe1andnhe6activitiesischemicandreperfusioninjury
bdutipo_str Repositorios
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