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Sodium loading raises urinary cortisol in man.

G Wambach, C Bleienheuft, G Bönner

    Journal of Endocrinological Investigation
    |June 1, 1986
    PubMed
    Summary
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    High sodium intake may alter kidney handling of cortisol, not affect pituitary-adrenal axis hormones like ACTH and cortisol. This study investigated the impact of dietary sodium on hormone levels.

    Area of Science:

    • Endocrinology
    • Renal Physiology
    • Hormone Regulation

    Background:

    • Dietary sodium intake is known to influence various physiological processes.
    • The relationship between sodium balance and the pituitary-adrenal axis, particularly cortisol metabolism, requires further elucidation.

    Purpose of the Study:

    • To investigate the effect of low versus high sodium intake on the diurnal rhythms of adrenocorticotropic hormone (ACTH) and cortisol.
    • To assess the impact of dietary sodium manipulation on urinary excretion of aldosterone and free cortisol.

    Main Methods:

    • Ten healthy subjects underwent a low sodium diet (40 mEq/day) for 4 days and a high sodium diet (320 mEq/day) for 6 days.
    • Serum ACTH and cortisol levels were measured every two hours over a 24-hour period at the end of each diet.

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  • Urinary aldosterone-18-glucuronide and free cortisol were quantified at the conclusion of each dietary phase.

    • Main Results:

    • Urinary aldosterone excretion significantly decreased on the low sodium diet compared to the high sodium diet.
    • Urinary free cortisol excretion increased during the high sodium intake period.
    • Diurnal patterns and levels of serum ACTH and cortisol remained comparable between the low and high sodium diet phases.

    Conclusions:

    • High sodium intake appears to alter renal handling of cortisol, leading to increased urinary free cortisol excretion.
    • The pituitary-adrenal axis, as indicated by ACTH and serum cortisol levels, does not show significant changes in response to short-term dietary sodium variations.
    • These findings suggest a dissociation between cortisol secretion/pulsatility and cortisol metabolism/excretion under different sodium loads.