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      Hypokalaemia induces Ca(2+) overload and Ca(2+) waves in ventricular myocytes by reducing Na(+),K(+)-ATPase α2 activity.

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          Abstract

          Hypokalaemia is a risk factor for development of ventricular arrhythmias. In rat ventricular myocytes, low extracellular K(+) (corresponding to clinical moderate hypokalaemia) increased Ca(2+) wave probability, Ca(2+) transient amplitude, sarcoplasmic reticulum (SR) Ca(2+) load and induced SR Ca(2+) 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(+), Ca(2+) exchanger (NCX) lead to increased Ca(2+) transient amplitude despite concomitant hyperpolarization of the resting membrane potential. Low extracellular K(+) induced Ca(2+) overload by lowering NKA α2 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 α2 isoform.

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          Author and article information

          Journal
          J. Physiol. (Lond.)
          The Journal of physiology
          Wiley-Blackwell
          1469-7793
          0022-3751
          Mar 15 2015
          : 593
          : 6
          Affiliations
          [1 ] Institute for Experimental Medical Research, Oslo University Hospital Ullevål and University of Oslo, Oslo, Norway; Bjørknes College, Oslo, Norway.
          Article
          10.1113/jphysiol.2014.279893
          4376427
          25772299
          305e5d5d-2b7d-4688-aac0-5df57280c932
          History

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