Send to

Choose Destination
See comment in PubMed Commons below
Pharmacol Ther. 2008 Sep;119(3):326-39. doi: 10.1016/j.pharmthera.2008.06.001. Epub 2008 Jul 1.

Pathophysiology and pharmacology of the cardiac "late sodium current.".

Author information

Dipartimento di Biotecnologie e Bioscienze, Università Milano-Bicocca Milano (IT), Italy.


The "late sodium current" (I(NaL)) is a sustained component of the fast Na+ current of cardiac myocytes and neurons. As recently appreciated, common neurological and cardiac conditions are associated with abnormal I(NaL) enhancement, which may contribute to the pathogenesis of both electrical and contractile dysfunction. For this reason, I(NaL) has become an appealing pharmacological target, with a potentially broad range of therapeutic indications. The recent approval by the FDA of an I(NaL) blocker (ranolazine) for clinical use justifies the increased interest in I(NaL) as a pathogenic mechanism and the rapid evolution of the information concerning it. The review focuses on cardiac aspects of I(NaL) enhancement; it deals with the origin of I(NaL), with its pathophysiological role and with the consequences of its pharmacological modulation. Both basic aspects and clinical evidence are discussed.

[Indexed for MEDLINE]
PubMed Commons home

PubMed Commons

How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science
    Loading ...
    Support Center