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10.1113/jphysiol.2014.279893 http://scihub22266oqcxt.onion/10.1113/jphysiol.2014.279893 C4376427!4376427!25772299     free     free     free Deprecated: Implicit conversion from float 225.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 225.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 225.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 225.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 225.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 225.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 225.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 259.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Physiol 2015 ; 593 (Pt 6): 1509-21 Nephropedia Template TP {{tp|p=25772299|t=2015. Hypokalaemia induces Ca2+ overload and Ca2+ waves in ventricular myocytes by reducing Na+,K+-ATPase ?2 activity |pdf=|usr=}}{{25772299}} gab.com Text Hypokalaemia induces Ca2+ overload and Ca2+ waves in ventricular myocytes by reducing Na+,K+-ATPase 2 activity JO: J Physiol http://www.kidney.de/pget.php?&tw=1&pmid=25772299 #FOAvip Hypokalaemia is a risk factor for development of ventricular arrhythmias. The aim of this study was to determine the cellular mechanisms leading to triggering of arrhythmias in ventricular myocytes exposed to low Ko. Low Ko, corresponding to moderate hypokalaemia, increased Ca2+ transient amplitude, sarcoplasmic reticulum (SR) Ca2+ load, SR Ca2+ leak and Ca2+ wave probability in field stimulated rat ventricular myocytes. The mechanisms leading to Ca2+ overload were examined. Low Ko reduced Na+,K+-ATPase (NKA) currents, increased cytosolic Na+ concentration and increased the Na+ level sensed by the Na+, Ca2+ exchanger (NCX). Low Ko also hyperpolarized the resting membrane potential (RMP) without significant alterations in action potential duration. Experiments in voltage clamped and field stimulated ventricular myocytes, along with mathematical modelling, suggested that low Ko increases the Ca2+ transient amplitude by reducing NKA activity despite hyperpolarization of the RMP. Selective inhibition of the NKA ?2 isoform by low dose ouabain abolished the ability of low Ko to reduce NKA currents, to increase Na+ levels sensed by NCX and to increase the Ca2+ transient amplitude. We conclude that low Ko, within the range of moderate hypokalaemia, increases Ca2+ levels in ventricular myocytes by reducing the pumping rate of the NKA ?2 isoform with subsequent Na+ accumulation sensed by the NCX. These data highlight reduced NKA ?2-mediated control of NCX activity as a possible mechanism underlying triggered ventricular arrhythmias in patients with hypokalaemia.Key points: Hypokalaemia is a risk factor for development of ventricular arrhythmias. In rat ventricular myocytes, low extracellular K+ (corresponding to clinical moderate hypokalaemia) increased Ca2+ wave probability, Ca2+ transient amplitude, sarcoplasmic reticulum (SR) Ca2+ load and induced SR Ca2+ leak. Low extracellular K+ reduced Na+,K+-ATPase (NKA) activity and hyperpolarized the resting membrane potential in ventricular myocytes. Both experimental data and modelling indicate that reduced NKA activity and subsequent Na+ accumulation sensed by the Na+, Ca2+ exchanger (NCX) lead to increased Ca2+ transient amplitude despite concomitant hyperpolarization of the resting membrane potential. Low extracellular K+ induced Ca2+ overload by lowering NKA ?2 activity. Triggered ventricular arrhythmias in patients with hypokalaemia may therefore be attributed to reduced NCX forward mode activity linked to an effect on the NKA ?2 isoform. Twit Text FOAVip Hypokalaemia induces Ca2+ overload and Ca2+ waves in ventricular myocytes by reducing Na+,K+-ATPase 2 activity ????J Physiol http://www.kidney.de/pget.php?&tw=1&pmid=25772299 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25772299 #FOAvip English Wikipedia <ref>{{Cite pmid|25772299}}</ref> Hypokalaemia induces Ca2+ overload and Ca2+ waves in ventricular myocytes by reducing Na+,K+-ATPase ?2 activity #MMPMID25772299 Aronsen JM; Skogestad J; Lewalle A; Louch WE; Hougen K; Stokke MK; Swift F; Niederer S; Smith NP; Sejersted OM; Sjaastad I J Physiol 2015[Mar]; 593 (Pt 6): 1509-21 PMID25772299show ga Hypokalaemia is a risk factor for development of ventricular arrhythmias. The aim of this study was to determine the cellular mechanisms leading to triggering of arrhythmias in ventricular myocytes exposed to low Ko. Low Ko, corresponding to moderate hypokalaemia, increased Ca2+ transient amplitude, sarcoplasmic reticulum (SR) Ca2+ load, SR Ca2+ leak and Ca2+ wave probability in field stimulated rat ventricular myocytes. The mechanisms leading to Ca2+ overload were examined. Low Ko reduced Na+,K+-ATPase (NKA) currents, increased cytosolic Na+ concentration and increased the Na+ level sensed by the Na+, Ca2+ exchanger (NCX). Low Ko also hyperpolarized the resting membrane potential (RMP) without significant alterations in action potential duration. Experiments in voltage clamped and field stimulated ventricular myocytes, along with mathematical modelling, suggested that low Ko increases the Ca2+ transient amplitude by reducing NKA activity despite hyperpolarization of the RMP. Selective inhibition of the NKA ?2 isoform by low dose ouabain abolished the ability of low Ko to reduce NKA currents, to increase Na+ levels sensed by NCX and to increase the Ca2+ transient amplitude. We conclude that low Ko, within the range of moderate hypokalaemia, increases Ca2+ levels in ventricular myocytes by reducing the pumping rate of the NKA ?2 isoform with subsequent Na+ accumulation sensed by the NCX. These data highlight reduced NKA ?2-mediated control of NCX activity as a possible mechanism underlying triggered ventricular arrhythmias in patients with hypokalaemia.Key points: Hypokalaemia is a risk factor for development of ventricular arrhythmias. In rat ventricular myocytes, low extracellular K+ (corresponding to clinical moderate hypokalaemia) increased Ca2+ wave probability, Ca2+ transient amplitude, sarcoplasmic reticulum (SR) Ca2+ load and induced SR Ca2+ leak. Low extracellular K+ reduced Na+,K+-ATPase (NKA) activity and hyperpolarized the resting membrane potential in ventricular myocytes. Both experimental data and modelling indicate that reduced NKA activity and subsequent Na+ accumulation sensed by the Na+, Ca2+ exchanger (NCX) lead to increased Ca2+ transient amplitude despite concomitant hyperpolarization of the resting membrane potential. Low extracellular K+ induced Ca2+ overload by lowering NKA ?2 activity. Triggered ventricular arrhythmias in patients with hypokalaemia may therefore be attributed to reduced NCX forward mode activity linked to an effect on the NKA ?2 isoform. äHypokalaemia induces Ca2+ overload and Ca2+ waves in ventricular myocy(epmc).pdf DeepDyve Pubget Overpricing