Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2008-9-8
pubmed:abstractText
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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0163-7258
pubmed:author
pubmed:issnType
Print
pubmed:volume
119
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
326-39
pubmed:meshHeading
pubmed:year
2008
pubmed:articleTitle
Pathophysiology and pharmacology of the cardiac "late sodium current.".
pubmed:affiliation
Dipartimento di Biotecnologie e Bioscienze, Università Milano-Bicocca Milano (IT), Italy. antonio.zaza@unimib.it
pubmed:publicationType
Journal Article, Review