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Related Experiment Videos

Digoxin-quinidine interaction: in vitro studies in rat tissue

C Kaplinsky, M Aladjem, N Wolfish

    The Journal of Laboratory and Clinical Medicine
    |October 1, 1980
    PubMed
    Summary

    Quinidine reduces digoxin uptake in kidney tissue by inhibiting an active transport mechanism. This interaction does not affect digoxin uptake in heart or muscle tissues, suggesting different transport pathways.

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    Area of Science:

    • Pharmacology
    • Renal Physiology
    • Drug Interactions

    Background:

    • Quinidine administration elevates serum digoxin levels in patients.
    • This interaction is hypothesized to involve digoxin displacement from tissues and reduced renal clearance.
    • Understanding the mechanism of this interaction is crucial for patient safety.

    Purpose of the Study:

    • To investigate the in vitro influence of quinidine on digoxin uptake by various rat tissues.
    • To determine if digoxin uptake is an active, energy-dependent process in renal tissue.
    • To elucidate the specific transport mechanisms involved in digoxin uptake in different tissues.

    Main Methods:

    • Utilized the in vitro tissue slice method to study 125I-digoxin uptake in rat kidney, heart, muscle, and fat tissues.

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  • Assessed the effect of quinidine addition to the incubation medium on digoxin uptake.
  • Investigated the impact of metabolic blockade (DNP, sodium azide) on digoxin uptake in kidney, heart, and muscle tissues.

    • Main Results:

    • Quinidine significantly reduced digoxin uptake in kidney tissue by 17.4% (p < 0.01).
    • Digoxin uptake in heart and striated muscle tissues was not affected by quinidine.
    • Metabolic blockade significantly reduced digoxin uptake in kidney slices, but not in heart or muscle tissues.

    Conclusions:

    • An active, energy-dependent transport mechanism for digoxin exists in renal cortical tissue.
    • This renal digoxin transport mechanism is inhibited by quinidine and metabolic blockers.
    • Digoxin uptake in heart and muscle tissues involves a different transport mechanism, unaffected by quinidine or metabolic inhibition.