We are analyzing https://link.springer.com/article/10.1007/s00395-017-0602-9.

Title:
Late sodium current and intracellular ionic homeostasis in acute ischemia | Basic Research in Cardiology
Description:
Blockade of the late Na+ current (I NaL) protects from ischemia/reperfusion damage; nevertheless, information on changes in I NaL during acute ischemia and their effect on intracellular milieu is missing. I NaL, cytosolic Na+ and Ca2+ activities (Nacyt, Cacyt) were measured in isolated rat ventricular myocytes during 7 min of simulated ischemia (ISC); in all the conditions tested, effects consistently exerted by ranolazine (RAN) and tetrodotoxin (TTX) were interpreted as due to I NaL blockade. The results indicate that I NaL was enhanced during ISC in spite of changes in action potential (AP) contour; I NaL significantly contributed to Nacyt rise, but only marginally to Cacyt rise. The impact of I NaL on Cacyt was markedly enhanced by blockade of the sarcolemmal(s) Na+/Ca2+ exchanger (NCX) and was due to the presence of (Na+-sensitive) Ca2+ efflux through mitochondrial NCX (mNCX). sNCX blockade increased Cacyt and decreased Nacyt, thus indicating that, throughout ISC, sNCX operated in the forward mode, in spite of the substantial Nacyt increment. Thus, a robust Ca2+ source, other than sNCX and including mitochondria, contributed to Cacyt during ISC. Most, but not all, of RAN effects were shared by TTX. (1) The paradigm that attributes Cacyt accumulation during acute ischemia to decrease/reversal of sNCX transport may not be of general applicability; (2) I NaL is enhanced during ISC, when the effect of Nacyt on mitochondrial Ca2+ transport may substantially contribute to I NaL impact on Cacyt; (3) RAN may act mostly, but not exclusively, through I NaL blockade during ISC.
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Keywords {🔍}

pubmed, article, google, scholar, cas, sodium, ventricular, ischemia, myocytes, late, ranolazine, current, pharmacol, res, central, nal, mitochondrial, intracellular, exchanger, reperfusion, cell, cardiol, cardiac, heart, zaza, rat, effects, mitochondria, injury, cardiovasc, myocardial, acute, ischemiareperfusion, cacyt, naca, role, calcium, mol, physiol, exchange, research, isolated, isc, circ, privacy, cookies, content, rocchetti, blockade, effect,

Topics {✒️}

marcella rocchetti & antonio zaza hydrogen peroxide-induced increases l-type ca2+ channels ischemia-induced carrier-mediated efflux month download article/chapter reverse-mode sodium/calcium exchange sodium/hydrogen exchange system late na+ current—origin intracellular ionic homeostasis myocardial ischemia-induced cytoplasmic na+-dependent ca2+ overload late sodium current anti-anginal drug ranolazine reverse na+/ca2+ exchange article basic research van rossum ac antonio zaza rat heart-underlying mechanisms late sodium channel late na+ current atp-sensitive potassium channel persistent sodium current inhibiting late na+ myocardial ischemia/reperfusion injury full article pdf cardiac ischemia/reperfusion injury mitochondrial ca2+ overload sodium-calcium exchanger wilms-schopman fj proton-gated ca ranolazine attenuates hypoxia privacy choices/manage cookies author information authors robust ca2+ source subcellular ca2+ distribution mitochondrial calcium uniporter acute ischaemia/reperfusion calcium release microdomains na+/ca2+ exchanger myocardial ionic currents sodium current mitochondrial ca2+ transport mitochondria regulate inactivation left ventricular myocytes improves mitochondrial integrity check access instant access single ventricular myocytes rat ventricular myocytes single cardiac myocytes

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         headline:Late sodium current and intracellular ionic homeostasis in acute ischemia
         description:Blockade of the late Na+ current (I NaL) protects from ischemia/reperfusion damage; nevertheless, information on changes in I NaL during acute ischemia and their effect on intracellular milieu is missing. I NaL, cytosolic Na+ and Ca2+ activities (Nacyt, Cacyt) were measured in isolated rat ventricular myocytes during 7 min of simulated ischemia (ISC); in all the conditions tested, effects consistently exerted by ranolazine (RAN) and tetrodotoxin (TTX) were interpreted as due to I NaL blockade. The results indicate that I NaL was enhanced during ISC in spite of changes in action potential (AP) contour; I NaL significantly contributed to Nacyt rise, but only marginally to Cacyt rise. The impact of I NaL on Cacyt was markedly enhanced by blockade of the sarcolemmal(s) Na+/Ca2+ exchanger (NCX) and was due to the presence of (Na+-sensitive) Ca2+ efflux through mitochondrial NCX (mNCX). sNCX blockade increased Cacyt and decreased Nacyt, thus indicating that, throughout ISC, sNCX operated in the forward mode, in spite of the substantial Nacyt increment. Thus, a robust Ca2+ source, other than sNCX and including mitochondria, contributed to Cacyt during ISC. Most, but not all, of RAN effects were shared by TTX. (1) The paradigm that attributes Cacyt accumulation during acute ischemia to decrease/reversal of sNCX transport may not be of general applicability; (2) I NaL is enhanced during ISC, when the effect of Nacyt on mitochondrial Ca2+ transport may substantially contribute to I NaL impact on Cacyt; (3) RAN may act mostly, but not exclusively, through I NaL blockade during ISC.
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            Late sodium current
            Ranolazine
            Na+ homeostasis
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            Mitochondria
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      description:Blockade of the late Na+ current (I NaL) protects from ischemia/reperfusion damage; nevertheless, information on changes in I NaL during acute ischemia and their effect on intracellular milieu is missing. I NaL, cytosolic Na+ and Ca2+ activities (Nacyt, Cacyt) were measured in isolated rat ventricular myocytes during 7 min of simulated ischemia (ISC); in all the conditions tested, effects consistently exerted by ranolazine (RAN) and tetrodotoxin (TTX) were interpreted as due to I NaL blockade. The results indicate that I NaL was enhanced during ISC in spite of changes in action potential (AP) contour; I NaL significantly contributed to Nacyt rise, but only marginally to Cacyt rise. The impact of I NaL on Cacyt was markedly enhanced by blockade of the sarcolemmal(s) Na+/Ca2+ exchanger (NCX) and was due to the presence of (Na+-sensitive) Ca2+ efflux through mitochondrial NCX (mNCX). sNCX blockade increased Cacyt and decreased Nacyt, thus indicating that, throughout ISC, sNCX operated in the forward mode, in spite of the substantial Nacyt increment. Thus, a robust Ca2+ source, other than sNCX and including mitochondria, contributed to Cacyt during ISC. Most, but not all, of RAN effects were shared by TTX. (1) The paradigm that attributes Cacyt accumulation during acute ischemia to decrease/reversal of sNCX transport may not be of general applicability; (2) I NaL is enhanced during ISC, when the effect of Nacyt on mitochondrial Ca2+ transport may substantially contribute to I NaL impact on Cacyt; (3) RAN may act mostly, but not exclusively, through I NaL blockade during ISC.
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