Cellular Mechanisms Underlying the Low Cardiotoxicity of Istaroxime

Background: Istaroxime is an inhibitor of Na⁺/K⁺ ATPase with proven efficacy to increase cardiac contractility and to accelerate relaxation attributable to a relief in phospholamban-dependent inhibition of the sarcoplasmic reticulum Ca²⁺ ATPase. We have previously shown that pharmacologic Na⁺/K⁺ ATP...

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Autores principales: Racioppi, María Florencia, Burgos Migone, Juan Ignacio, Morell, Malena, Gonano, Luis Alberto, Vila Petroff, Martín Gerardo
Formato: Articulo
Lenguaje:Inglés
Publicado: 2021
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Acceso en línea:http://sedici.unlp.edu.ar/handle/10915/136866
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id I19-R120-10915-136866
record_format dspace
institution Universidad Nacional de La Plata
institution_str I-19
repository_str R-120
collection SEDICI (UNLP)
language Inglés
topic Medicina
Ca2+/calmodulin-dependent kinase II
cardiotoxicity
digitalis and apoptosis
istaroxime
spellingShingle Medicina
Ca2+/calmodulin-dependent kinase II
cardiotoxicity
digitalis and apoptosis
istaroxime
Racioppi, María Florencia
Burgos Migone, Juan Ignacio
Morell, Malena
Gonano, Luis Alberto
Vila Petroff, Martín Gerardo
Cellular Mechanisms Underlying the Low Cardiotoxicity of Istaroxime
topic_facet Medicina
Ca2+/calmodulin-dependent kinase II
cardiotoxicity
digitalis and apoptosis
istaroxime
description Background: Istaroxime is an inhibitor of Na⁺/K⁺ ATPase with proven efficacy to increase cardiac contractility and to accelerate relaxation attributable to a relief in phospholamban-dependent inhibition of the sarcoplasmic reticulum Ca²⁺ ATPase. We have previously shown that pharmacologic Na⁺/K⁺ ATPase inhibition promotes calcium/calmodulin-dependent kinase II activation, which mediates both cardiomyocyte death and arrhythmias. Here, we aim to compare the cardiotoxic effects promoted by classic pharmacologic Na⁺/K⁺ ATPase inhibition versus istaroxime. Methods and results: Ventricular cardiomyocytes were treated with ouabain or istaroxime at previously tested equi-inotropic concentrations to compare their impact on cell viability, apoptosis, and calcium/calmodulin-dependent kinase II activation. In contrast to ouabain, istaroxime neither promoted calcium/calmodulin-dependent kinase II activation nor cardiomyocyte death. In addition, we explored the differential behavior promoted by ouabain and istaroxime on spontaneous diastolic Ca²⁺ release. In rat cardiomyocytes, istaroxime did not significantly increase Ca²⁺ spark and wave frequency but increased the proportion of aborted Ca²⁺ waves. Further insight was provided by studying cardiomyocytes from mice that do not express phospholamban. In this model, the lower Ca²⁺ wave incidence observed with istaroxime remains present, suggesting that istaroxime-dependent relief on phospholamban-dependent sarcoplasmic reticulum Ca²⁺ ATPase 2A inhibition is not the unique mechanism underlying the low arrhythmogenic profile of this drug. Conclusions: Our results indicate that, different from ouabain, istaroxime can reach a significant inotropic effect without leading to calcium/calmodulin-dependent kinase II–dependent cardiomyocyte death. Additionally, we provide novel insights regarding the low arrhythmogenic impact of istaroxime on cardiac Ca²⁺ handling.
format Articulo
Articulo
author Racioppi, María Florencia
Burgos Migone, Juan Ignacio
Morell, Malena
Gonano, Luis Alberto
Vila Petroff, Martín Gerardo
author_facet Racioppi, María Florencia
Burgos Migone, Juan Ignacio
Morell, Malena
Gonano, Luis Alberto
Vila Petroff, Martín Gerardo
author_sort Racioppi, María Florencia
title Cellular Mechanisms Underlying the Low Cardiotoxicity of Istaroxime
title_short Cellular Mechanisms Underlying the Low Cardiotoxicity of Istaroxime
title_full Cellular Mechanisms Underlying the Low Cardiotoxicity of Istaroxime
title_fullStr Cellular Mechanisms Underlying the Low Cardiotoxicity of Istaroxime
title_full_unstemmed Cellular Mechanisms Underlying the Low Cardiotoxicity of Istaroxime
title_sort cellular mechanisms underlying the low cardiotoxicity of istaroxime
publishDate 2021
url http://sedici.unlp.edu.ar/handle/10915/136866
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