The endogenous ouabain: Molecular basis of its role in hypertension and cardiovascular complications

Mara Ferrandi, Paolo Manunta, Patrizia Ferrari, Giuseppe Bianchi

Research output: Contribution to journalArticlepeer-review


Elevated levels of the endogenous ouabain (EO), a closely related isomer of ouabain, are implicated in rat and human hypertension and in related cardiovascular complications. The pathogenetic mechanisms through which EO affects the cardiovascular system involve the modulation of the renal Na/K-ATPase, implicated in renal tubular sodium reabsorption, and the activation of signal transduction pathways, promoting the transcription of growth-related genes. Experimental and clinical evidence on rats and humans stimulated the pharmacological research for developing novel anti-hypertensive agents able to antagonize the cellular and molecular alterations mediated by EO. Among them, the digitoxigenin derivate, PST 2238, has been selected for its ability to antagonize the ouabain-induced effects on blood pressure and organ hypertrophy at oral doses of μg/kg/day in vivo. The pharmacological selectivity and safety of PST 2238 suggests that the compound may be effective for the treatment of those forms of hypertension in which renal sodium handling alterations and cardiovascular complications are associated with increased production of EO.

Original languageEnglish
Pages (from-to)2472-2477
Number of pages6
JournalFrontiers in Bioscience
Issue numberSUPPL. 2
Publication statusPublished - 2005


  • Adducin
  • Endogenous Ouabain
  • Genetic
  • Hypertension
  • Hypertrophy
  • Na, K, Atpase
  • Rat
  • Review

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)
  • Biochemistry
  • Cell Biology


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