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Related Experiment Videos

Antihypertensive compounds that modulate the Na-K pump.

P Ferrari1, M Ferrandi, L Torielli

  • 1Prassis Research Institute, Sigma Tau, Milan, Italy. patrizia.ferrari@prassis.it

Annals of the New York Academy of Sciences
|May 24, 2003
PubMed
Summary

A novel antihypertensive agent, PST 2238, effectively lowers blood pressure by normalizing renal Na-K pump activity in models of hypertension. It also prevents cardiac and kidney hypertrophy linked to endogenous ouabain.

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Area of Science:

  • Nephrology
  • Cardiology
  • Pharmacology

Background:

  • Hypertension is linked to impaired kidney sodium excretion, associated with adducin mutations or increased endogenous ouabain (EO).
  • Endogenous ouabain (EO) and mutated adducin activate renal Na/K-ATPase, contributing to hypertension and potential cardiac complications.

Purpose of the Study:

  • To develop and evaluate a novel antihypertensive agent, PST 2238, targeting specific alterations in renal Na/K-ATPase function.
  • To assess PST 2238's efficacy in normalizing blood pressure and preventing cardiovascular complications in hypertensive models.

Main Methods:

  • PST 2238 was administered orally to genetic rat models (MHS, OS) and tested in cultured renal cells (NRK) with mutated adducin or EO.
  • Effects on blood pressure, renal Na-K pump expression/activity, and cardiac/kidney weights were measured.

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  • Gene expression related to OU-dependent growth pathways was analyzed.

    • Main Results:

    • PST 2238 lowered blood pressure in MHS and OS rats at low oral doses (0.1-10 micro g/kg).
    • PST 2238 normalized Na-K pump activity in cultured cells and in vivo.
    • PST 2238 prevented left ventricle and kidney hypertrophy in OS rats by antagonizing EO-induced gene activation.

    Conclusions:

    • PST 2238 is a novel antihypertensive agent with selective action on the renal Na-K pump.
    • PST 2238 demonstrates potential in preventing hypertension-associated cardiovascular complications.
    • The drug's mechanism involves modulating Na-K pump function and inhibiting OU-dependent growth pathways.