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Related Experiment Videos

Ranitidine treatment and cortisol metabolism in man.

H Mönig1, K Hoffmann, E E Ohnhaus

  • 11. Medizinische Klinik der Christian-Albrechts-Universität, Kiel, Germany.

European Journal of Drug Metabolism and Pharmacokinetics
|January 1, 1992
PubMed
Summary

Ranitidine, a common H2-receptor antagonist, does not significantly impact cortisol metabolism or antipyrine clearance in healthy individuals. This study found no substantial effects on adrenal corticosteroid production or hepatic drug metabolism.

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Area of Science:

  • Pharmacology
  • Drug Metabolism
  • Endocrinology

Background:

  • H2-receptor antagonists, like ranitidine, are widely used medications.
  • Experimental data suggested potential inhibition of cytochrome P-450 enzymes by H2-receptor antagonists.
  • Cytochrome P-450 enzymes are crucial for drug and hormone metabolism in the liver and adrenal glands.

Purpose of the Study:

  • To investigate the effects of ranitidine on cortisol metabolism.
  • To assess the impact of ranitidine on antipyrine clearance.
  • To determine if ranitidine affects hepatic and adrenal cytochrome P-450 dependent monooxygenases.

Main Methods:

  • Nine healthy volunteers received ranitidine (150 mg twice daily) for 14 days.
  • Urinary excretion of 6 beta-hydroxycortisol (6 beta-OHC) and 17-hydroxycorticosteroids (17-OHCS) was measured.

Related Experiment Videos

  • Antipyrine kinetics and metabolite formation were analyzed.

    • Main Results:

    • Ranitidine did not alter the urinary excretion of 6 beta-hydroxycortisol or 17-hydroxycorticosteroids.
    • The 6 beta-OHC/17-OHCS ratio remained unchanged, indicating no effect on cortisol metabolism.
    • Antipyrine clearance and metabolite formation showed only marginal changes.

    Conclusions:

    • Ranitidine administration does not significantly affect adrenal corticosteroid production.
    • Hepatic metabolism of cortisol is not influenced by ranitidine.
    • Ranitidine appears to have minimal impact on cytochrome P-450 mediated drug metabolism in humans.