The Late Sodium Current and the Therapeutic Consequences of its Pharmacological Blockade

来源 :BITs 2rd Annual World Cancer Congress of Cardiology-2010(201 | 被引量 : 0次 | 上传用户:ineedtoxiazai
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  The "late sodium current" (late INa) is a sustained component of the fast Na+ current of cardiac myocytes.It is due to the lack of inactivation or to late reopening of the voltage-gated Na+ channels.Late INa is increased under pathological conditions, such as ischaemia.Enhancement of Na+ influx through late INa increases cytosolic Na+ concentration, which on its turn reduces Ca2+ efflux via the cell membrane sodium-calcium exchanger (NCX).Hence, entry of Ca2+ into the myocardial cell via NCX may exceed Ca2+ effiux and precipitate Ca2+ overload with mechanical and electrical consequences.Ranolazine is a selective inhibitor of late INa exerting anti-ischcmic and antianginal effects.The evidence that ranolazine, at concentrations within its therapeutic range (-3d10 μM), significantly reduces late INa and reverses or prevents the consequences of an increase of late INa will be presented.
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