Digitalis: New actions for an old drug

J. Andrew Wasserstrom*, Gary L. Aistrup

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

105 Scopus citations


The mechanisms by which digitalis causes its therapeutic and toxic actions have been studied for nearly a half century, revealing a great deal about cardiac cell regulation of intracellular ions via the Na-K-ATPase (NKA) and how it is altered by cardiac glycosides. However, recent observations suggest that digitalis may have additional effects on cardiac cell function in both the short and long term that include intracellular effects, interactions with specific NKA isoforms in different cellular locations, effects on intracellular (including nuclear) signaling, and long-term regulation of intracellular ionic balances through circulating ouabain-like compounds. The purpose of this review is to examine the current status of a number of the newest and most interesting developments in the study of digitalis with a particular focus on cardiac function, although we will also discuss some of the new advances in other relevant cardiovascular effects. This new information has important implications for both our understanding of ionic regulation in normal and diseased hearts as well as for potential avenues for the development of future therapeutic interventions for the treatment of heart failure.

Original languageEnglish (US)
Pages (from-to)H1781-H1793
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Issue number5 58-5
StatePublished - Nov 2005


  • Cardiac glycosides
  • Digoxin
  • Excitation-contraction coupling
  • Mitogen-activated protein kinase
  • Ouabain
  • Ouabain-like compound
  • Sarcoplasmic reticulum
  • Sodium-potassium adenosinetriphosphatase

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

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