Cardiac glycosides and intracellular Na+, K+, Ca2+.

Item request has been placed! ×
Item request cannot be made. ×
loading   Processing Request
Read More Add to Saved list
  • Author(s): Noack E
  • Source:
    Basic research in cardiology [Basic Res Cardiol] 1984; Vol. 79 Suppl, pp. 87-92.
  • Publication Type:
    Journal Article
  • Language:
    English
  • Additional Information
    • Source:
      Publisher: Steinkopff Country of Publication: Germany NLM ID: 0360342 Publication Model: Print Cited Medium: Print ISSN: 0300-8428 (Print) Linking ISSN: 03008428 NLM ISO Abbreviation: Basic Res Cardiol Subsets: MEDLINE
    • Publication Information:
      Original Publication: Darmstadt, Steinkopff.
    • Subject Terms:
      Calcium/*analysis ; Cardiac Glycosides/*pharmacology ; Myocardial Contraction/*drug effects ; Myocardium/*analysis ; Potassium/*analysis ; Sodium/*analysis; Animals ; Biological Transport, Active/drug effects ; Cardiac Glycosides/toxicity ; Guinea Pigs ; Intracellular Fluid/analysis ; Rabbits ; Sodium-Potassium-Exchanging ATPase/antagonists & inhibitors ; Stimulation, Chemical
    • Abstract:
      From the fact that cardiac glycosides exert their positive inotropy most likely via a concentration-dependent inhibition of the Na+/K+-activated ATPase, a membrane-bound enzyme regulating the intracellular potassium and sodium homeostasis, one might assume that intracellular electrolyte changes may be easily detectable. Just the opposite holds true. In the literature there are very conflicting observations depending on the experimental model, the analytical method used etc. At the moment, nevertheless, there is great body of evidence that if the cardiac glycoside inotropy is mediated by an inhibition of Na+/K+-activated ATPase this is not accompanied by a measurable alteration of intracellular ionic composition. On the other hand toxic concentrations of cardiac glycosides significantly produce a loss of cellular potassium and a rise of cellular sodium and calcium content, especially if arrhythmias are present. The increase of intracellular free and bound calcium, which manifests itself functionally as contracture, is believed to be caused at least by two mechanisms: a stimulation of the Na-Ca-exchange and an inhibition of the specific Ca2+-activated ATPase in the plasma membrane catalyzing the uphill Ca2+ outward transport. In vitro studies show that this process is impeded by a local rise of the sodium ion concentration. As the determination of myocardial ion fluxes and cellular electrolyte content has its experimental limitations, further insight may be gained by new techniques which give an answer about possible changes of the electrolyte balance at the subcellular level.
    • Accession Number:
      0 (Cardiac Glycosides)
      9NEZ333N27 (Sodium)
      EC 7.2.2.13 (Sodium-Potassium-Exchanging ATPase)
      RWP5GA015D (Potassium)
      SY7Q814VUP (Calcium)
    • Publication Date:
      Date Created: 19840101 Date Completed: 19840802 Latest Revision: 20191210
    • Publication Date:
      20221213
    • Accession Number:
      10.1007/978-3-642-72376-6_12
    • Accession Number:
      6331382