Role of [Na+]i and the emerging involvement of the late sodium current in the pathophysiology of cardiovascular disease
Abt. Kardiologie and Pneumologie/Herzzentrum, Georg-August-Universität Göttingen, Robert-Koch-Str. 40, 37075 Göttingen, Germany
* Corresponding author. Tel: +49 551 39 9481; fax: +49 551 39 8941. E-mail address: lmaier{at}med.uni-goettingen.de
In recent years, it has become increasingly clear that, as well as abnormal intracellular calcium handling, changes in intracellular sodium homeostasis play an important role in the pathophysiology of heart failure. One key source of altered sodium homeostasis may be the slow inactivating sodium current. Altered intracellular sodium promotes alterations in intracellular calcium mainly through the sarcolemmal Na+/Ca2+ exchanger that can transport Ca2+ vs. Na+ in both directions. Changes in both calcium and sodium handling are the main factors associated with cardiac dysfunction and the propensity for cardiac arrhythmias. This article gives insight into the mechanisms involved in the pathophysiology of sodium homeostasis in heart failure.
Key Words: Late sodium current Heart failure Excitationcontraction coupling Calcium/calmodulin-dependent protein kinase II