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Calcium-calmodulin kinase II mediates digitalis-induced arrhythmias

Gonano, Luis AlbertoIcon ; Sepúlveda, Marisa NoemíIcon ; Rico, Yanina Vanesa; Kaetzel, Marcia; Valverde, Carlos AlfredoIcon ; Dedman, John; Mattiazzi, Ramona AliciaIcon ; Vila Petroff, Martin GerardeIcon
Fecha de publicación: 12 - 2011
Editorial: Lippincott Williams
Revista: Circulation-arrhythmia And Electrophysiology
Idioma: Inglés
URI: http://hdl.handle.net/11336/60874
https://www.ahajournals.org/doi/abs/10.1161/CIRCEP.111.964908?url_ver=Z39.88-200
http://dx.doi.org/10.1161/CIRCEP.111.964908
Citación: Gonano, Luis Alberto; Sepúlveda, Marisa Noemí; Rico, Yanina Vanesa; Kaetzel, Marcia; Valverde, Carlos Alfredo; et al.; Calcium-calmodulin kinase II mediates digitalis-induced arrhythmias; Lippincott Williams; Circulation-arrhythmia And Electrophysiology; 4; 6; 12-2011; 947-957

Abstract

Digitalis-induced Na(+) accumulation results in an increase in Ca(2+)(i) via the Na(+)/Ca(2+) exchanger, leading to enhanced sarcoplasmic reticulum (SR) Ca(2+) load, responsible for the positive inotropic and toxic arrhythmogenic effects of glycosides. A digitalis-induced increase in Ca(2+)(i) could also activate calcium-calmodulin kinase II (CaMKII), which has been shown to have proarrhythmic effects. Here, we investigate whether CaMKII underlies digitalis-induced arrhythmias and the subcellular mechanisms involved.

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info:eu-repo/semantics/restrictedAccess Excepto donde se diga explícitamente, este item se publica bajo la siguiente descripción: Creative Commons Attribution-NonCommercial-ShareAlike 2.5 Unported (CC BY-NC-SA 2.5)
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