Display options
Cite
Kjeldsen K. Myocardial Na,K-ATPase: Clinical aspects. Exp Clin Cardiol. 2003;8(3):131-3
Kjeldsen, K. (2003). Myocardial Na,K-ATPase: Clinical aspects. Experimental and clinical cardiology, 8(3), 131-3.
Kjeldsen, Keld. "Myocardial Na,K-ATPase: Clinical aspects." Experimental and clinical cardiology vol. 8,3 (2003): 131-3.
Kjeldsen K. Myocardial Na,K-ATPase: Clinical aspects. Exp Clin Cardiol. 2003;8(3):131-3. PMID: 19641704; PMCID: PMC2716273.
Copy Download .nbib Format: NLM
Share it on

Exp Clin Cardiol. 2003;8(3):131-3.

Myocardial Na,K-ATPase: Clinical aspects.

Experimental and clinical cardiology

Keld Kjeldsen

Affiliations

  1. Laboratory for Molecular Cardiology, Copenhagen Heart Arrhythmia Research Centre, The Heart Centre, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark.

PMID: 19641704 PMCID: PMC2716273

Abstract

The specific binding of digitalis glycosides to Na,K-ATPase is used as a tool for Na,K-ATPase quantification with high accuracy and precision. In myocardial biopsies from patients with heart failure, total Na,K-ATPase concentration is decreased by around 40%; a correlation exists between a decrease in heart function and a decrease in Na,K-ATPase concentration. During digitalization, around 30% of remaining pumps are occupied by digoxin. Myocardial Na,K-ATPase is also influenced by other drugs used for the treatment of heart failure. Thus, potassium loss during diuretic therapy has been found to reduce myocardial Na,K-ATPase, whereas angiotensin-converting enzyme inhibitors may stimulate Na,K pump activity. Furthermore, hyperaldosteronism induced by heart failure has been found to decrease Na,K-ATPase activity. Accordingly, treatment with the aldosterone antagonist, spironolactone, may also influence Na,K-ATPase activity. The importance of Na,K pump modulation with heart disease, inhibition in digitalization and other effects of medication should be considered in the context of sodium, potassium and calcium regulation. It is recommended that digoxin be administered to heart failure patients who, after institution of mortality-reducing therapy, still have heart failure symptoms, and that the therapy be continued if symptoms are revealed or reduced. Digitalis glycosides are the only safe inotropic drugs for oral use that improve hemodynamics in heart failure.An important aspect of myocardial Na,K pump affection in heart disease is its influence on extracellular potassium (K(e)) homeostasis. Two important aspects should be considered: potassium handling among myocytes, and effects of potassium entering the extracellular space of the heart via the bloodstream. It should be noted that both of these aspects of K(e) homeostasis are affected by regulatory aspects, eg, regulation of the Na,K pump by physiological and pathophysiological conditions, as well as by medical treatments. Digitalization has been shown to affect both parameters. Furthermore, in experimental animals, potassium loading and depletion are found to significantly affect K(e) handling. The effects of potassium depletion are of special interest because this condition often occurs in patients treated with diuretics. In human congenital long QT syndrome caused by mutations in genes coding for potassium channels, exercise and potassium depletion are well known for their potential to elicit arrhythmias and sudden death. There is a need for further evaluation of the dynamic aspects of potassium handling in the heart, as well as in the periphery. It is recommended that resting plasma potassium be maintained at around 4 mmol/L.

Keywords: Digoxin; Heart; Na, K-ATPase; Potassium

References

  1. Cardiovasc Res. 1988 Feb;22(2):95-100 - PubMed
  2. Arch Intern Med. 2000 Sep 11;160(16):2429-36 - PubMed
  3. J Physiol. 1987 Jul;388:163-81 - PubMed
  4. J Appl Physiol (1985). 1993 Jul;75(1):173-80 - PubMed
  5. Am J Physiol. 1988 Jan;254(1 Pt 1):C1-7 - PubMed
  6. N Engl J Med. 1997 Feb 20;336(8):525-33 - PubMed
  7. Helv Physiol Pharmacol Acta. 1953;11(4):346-54 - PubMed
  8. Heart. 2001 Jul;86(1):12-4 - PubMed
  9. News Physiol Sci. 2000 Aug;15:176-180 - PubMed
  10. Cardiovasc Res. 1970 Apr;4(2):201-6 - PubMed
  11. J Hypertens. 1993 Jul;11(7):683-91 - PubMed
  12. Am J Cardiol. 1988 Jun 1;61(15):1312-5 - PubMed
  13. Basic Res Cardiol. 1992;87 Suppl 1:87-94 - PubMed
  14. Cardiovasc Res. 2002 Sep;55(4):710-3 - PubMed
  15. Mol Cell. 1999 May;3(5):555-63 - PubMed
  16. Cardiovasc Res. 1993 Dec;27(12):2229-37 - PubMed
  17. Br J Cancer. 2003 Nov 3;89(9):1633-7 - PubMed
  18. Circulation. 2002 May 28;105(21):2543-8 - PubMed
  19. Circulation. 1998 Jan 27;97(3):282-9 - PubMed
  20. J Mol Cell Cardiol. 1998 Oct;30(10):2037-46 - PubMed
  21. FEBS Lett. 1996 Apr 15;384(2):203-5 - PubMed
  22. J Pharmacol Exp Ther. 1985 Dec;235(3):629-35 - PubMed
  23. Am J Cardiol. 1999 Feb 1;83(3):396-9 - PubMed
  24. J Appl Physiol (1985). 2003 Oct;95(4):1606-16 - PubMed
  25. Am J Physiol Cell Physiol. 2002 Oct;283(4):C1163-70 - PubMed
  26. Circ Res. 2000 Jan 7-21;86(1):37-42 - PubMed
  27. Cardiovasc Res. 1991 Aug;25(8):684-91 - PubMed
  28. J Cardiovasc Pharmacol. 1990 May;15(5):692-7 - PubMed
  29. Circulation. 1999 Apr 27;99(16):2105-12 - PubMed
  30. Cardiovasc Res. 1995 Apr;29(4):506-11 - PubMed
  31. Circulation. 2002 Jul 23;106(4):447-53 - PubMed
  32. Circulation. 1972 Jan;45(1):107-13 - PubMed
  33. Br Med J (Clin Res Ed). 1988 Feb 13;296(6620):455-8 - PubMed
  34. Circulation. 2000 Feb 15;101(6):616-23 - PubMed
  35. Nature. 2003 Feb 6;421(6923):634-9 - PubMed
  36. Am J Physiol. 1995 Feb;268(2 Pt 1):C366-75 - PubMed
  37. Clin Sci (Lond). 1998 Jul;95(1):3-17 - PubMed
  38. J Cardiovasc Pharmacol. 1992 Apr;19(4):554-61 - PubMed
  39. Am J Med. 2001 Apr 1;110(5):385-98 - PubMed
  40. Am J Cardiol. 1993 Jan 1;71(1):110-4 - PubMed
  41. J Appl Physiol (1985). 1997 Apr;82(4):1136-44 - PubMed
  42. Circulation. 1996 Sep 1;94(5):1018-22 - PubMed

Publication Types