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Sodium transport and red cell deformability.

G Wambach, U Overhoff, V Hossmann

    Klinische Wochenschrift
    |January 1, 1985
    PubMed
    Summary
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    Digoxin inhibits the sodium-potassium pump (Na-K pump), reducing red blood cell (RBC) deformability in lab tests. However, this effect was not observed in healthy volunteers at therapeutic doses, suggesting it occurs only at toxic levels.

    Area of Science:

    • Cardiovascular Physiology
    • Hematology
    • Pharmacology

    Background:

    • The sodium-potassium pump (Na-K pump) plays a crucial role in cardiovascular health.
    • Dysfunction of the Na-K pump is implicated in the development of essential hypertension.
    • Circulating factors inhibiting the Na-K pump are hypothesized to contribute to hypertension pathophysiology.

    Purpose of the Study:

    • To investigate the relationship between Na-K pump inhibition by digoxin and red blood cell (RBC) deformability.
    • To assess this correlation both in vitro and in vivo.

    Main Methods:

    • Erythrocytes were incubated with varying concentrations of digoxin (0-1.3 mumol/l) at 37°C for 1 hour.
    • Na-K pump activity was measured by 86rubidium (Rb) uptake.
    • Red blood cell filtrability was assessed.

    Related Experiment Videos

  • Nine healthy volunteers ingested digoxin (0.2 mg twice daily) for 5 days.

    • Main Results:

    • In vitro, high digoxin concentrations (0.13 and 1.3 mumol/l) significantly reduced Na-K pump activity and red cell filtrability.
    • In vivo, digoxin administration to healthy volunteers did not alter RBC deformability or Na-K pump activity (86Rb uptake).
    • The observed in vitro effects on RBC deformability occurred at toxic digoxin concentrations.

    Conclusions:

    • In vitro, Na-K pump inhibition by digoxin correlates with decreased red blood cell deformability.
    • This correlation is only evident at toxic doses of digoxin.
    • The study suggests that Na-K pump inhibition's effect on RBC deformability may not be significant at therapeutic digoxin levels in vivo.