Key result
Altered cardiac sodium current drives intracellular sodium loading in hypertrophy, ischemia, and heart failure.
Why the study?
Alterations in the cardiac Na current in acquired diseases such as hypertrophy, failure, and ischemia affect sodium loading and intracellular Na homeostasis, necessitating a detailed review of the human ventricular Na channel structure and function.
Answers are grounded in this paper and cite their sources.
This review highlights the structure and function of the human cardiac Na channel and its role in sodium loading and homeostasis in acquired cardiac diseases such as hypertrophy, failure, and ischemia.
The Na current (I(Na)) in human ventricle is carried through a specific isoform of the voltage gated Na channel in heart. The pore forming alpha-subunit is encoded by the gene SCN5A. Up to four beta-subunits may be associated, and the larger macromolecular complex may include attachments to cytoskeleton and scaffolding proteins, all of which may affect the gating kinetics of the current. I(Na) underlies initiation and propagation of action potentials in the heart and plays a prominent role in cardiac electrophysiology and arrhythmia. In addition, I(Na) also loads the ventricular cell with Na(+) ions and plays an important role in intracellular Na homeostasis. This review considers the structure and function of the human cardiac Na channel that carries I(Na) with a particular consideration of the implications of alterations in I(Na) in acquired cardiac diseases such as hypertrophy, failure, and ischemia, which affect Na loading.
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Makielski et al. (2006) conducted a review in Acquired cardiac diseases (hypertrophy, failure, ischemia). Na+ current (I(Na)) alterations was evaluated. Alterations in the human cardiac Na+ current (I(Na)) play a significant role in intracellular sodium loading and homeostasis in acquired cardiac diseases such as hypertrophy, failure, and ischemia.
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