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Cardiovascular Research 2007 73(4):648-656; doi:10.1016/j.cardiores.2006.12.002
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Copyright © 2006, European Society of Cardiology

Ca2+/calmodulin-dependent protein kinase: A key component in the contractile recovery from acidosis

Alicia Mattiazzi*, Leticia Vittone and Cecilia Mundiña-Weilenmann

Centro de Investigaciones Cardiovasculares, Facultad de Ciencias Médicas, Universidad Nacional de La Plata, 60 y 120. (1900) La Plata, Argentina

* Corresponding author. Tel.: +54 221 489 4813; fax: +54 221 483 4833. Email address: ramattia{at}atlas.med.unlp.edu.ar

Intracellular acidosis exerts substantial effects on the contractile performance of the heart. Soon after the onset of acidosis, contractility diminishes, largely due to a decrease in myofilament Ca2+ responsiveness. This decrease in contractility is followed by a progressive recovery that occurs despite the persistent acidosis. This recovery is the result of different mechanisms that converge to increase diastolic Ca2+ levels and Ca2+ transient amplitude. Recent experimental evidence indicates that activation of the Ca2+/calmodulin-dependent protein kinase II (CaMKII) is an essential step in the sequence of events that increases the Ca2+ transient amplitude and produces contractile recovery. CaMKII may act as an amplifier, providing compensatory pathways to offset the inhibitory effects of acidosis on many of the Ca2+ handling proteins. CaMKII-induced phosphorylation of the SERCA2a regulatory protein phospholamban (PLN) has the potential to promote an increase in sarcoplasmic reticulum (SR) Ca2+ uptake and SR Ca2+ load, and is a likely candidate to mediate the mechanical recovery from acidosis. In addition, CaMKII-dependent phosphorylation of proteins other than PLN may also contribute to this recovery.

KEYWORDS Acidosis; CaMKII; Protein phosphorylation; SR function

Time for primary review 14 days


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