Mineralocorticoid receptor activation following acute myocardial stretch

Myocardial stretch induces a two-phase increase in developed force. The first phase occurs immediately, is due to an increase in myofilament Ca2+ responsiveness, and is the expression of the Frank-Starling mechanism. The second phase, gradually developed, results from an increase in intracellular Ca...

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Autor principal: Pérez, Néstor Gustavo
Formato: Articulo
Lenguaje:Inglés
Publicado: 2017
Materias:
Ciencias Médicas
Mineralocorticoid receptor
Myocardial stretch
Clinical impact
Acceso en línea:http://sedici.unlp.edu.ar/handle/10915/104363
http://hdl.handle.net/11336/49490
Aporte de:
SEDICI (UNLP) de Universidad Nacional de La Plata
id I19-R120-10915-104363
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
Mineralocorticoid receptor
Myocardial stretch
Clinical impact
spellingShingle Ciencias Médicas
Mineralocorticoid receptor
Myocardial stretch
Clinical impact
Pérez, Néstor Gustavo
Mineralocorticoid receptor activation following acute myocardial stretch
topic_facet Ciencias Médicas
Mineralocorticoid receptor
Myocardial stretch
Clinical impact
description Myocardial stretch induces a two-phase increase in developed force. The first phase occurs immediately, is due to an increase in myofilament Ca2+ responsiveness, and is the expression of the Frank-Starling mechanism. The second phase, gradually developed, results from an increase in intracellular Ca2+ concentration and is known as ?slow force response? (SFR) to stretch. Characterization of the subcellular basis of the increase in Ca2+ responsible for the SFR development was an important objective of our laboratory group during last two decades. We have compiled enough evidence to suggest that the SFR is the mechanical expression of an autocrine/paracrine loop of intracellular signals leading to the reactive oxygen species (ROS)-mediated activation of redox-sensitive kinases that activate (phosphorylate) the cardiac Na+/H+ exchanger (NHE1), increasing intracellular Na+, and consequently, Ca2+ concentration. Recently, we demonstrated that mineralocorticoid receptor (MR) activation after stretch is critical for the progression of this complex signaling pathway. Interestingly, clinical evidence assigns a detrimental role to MR activation in the pathophysiology of heart failure (HF), in which cardiac wall stretch is an important triggering factor. The aim of this mini-review is not only to share our own experience describing novel non-genomic effects of MR activation after acute myocardial stretch and the physiological consequences, but also to discuss other possible pathophysiological implications, as well as the potential clinical impact of this important discovery.
format Articulo
Articulo
author Pérez, Néstor Gustavo
author_facet Pérez, Néstor Gustavo
author_sort Pérez, Néstor Gustavo
title Mineralocorticoid receptor activation following acute myocardial stretch
title_short Mineralocorticoid receptor activation following acute myocardial stretch
title_full Mineralocorticoid receptor activation following acute myocardial stretch
title_fullStr Mineralocorticoid receptor activation following acute myocardial stretch
title_full_unstemmed Mineralocorticoid receptor activation following acute myocardial stretch
title_sort mineralocorticoid receptor activation following acute myocardial stretch
publishDate 2017
url http://sedici.unlp.edu.ar/handle/10915/104363
http://hdl.handle.net/11336/49490
work_keys_str_mv AT pereznestorgustavo mineralocorticoidreceptoractivationfollowingacutemyocardialstretch
bdutipo_str Repositorios
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