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Adrenocortical function and plasma norepinephrine in normal human subjects

S M Sotsky, C R Lake, F K Goodwin

    Biological Psychiatry
    |July 1, 1981
    PubMed
    Summary
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    This study suggests norepinephrine (NE) inhibits the hypothalamic-pituitary adrenal (HPA) axis, and cortisol may reciprocally affect noradrenergic activity. These findings offer insights into adrenocortical regulation in depression.

    Area of Science:

    • Neuroendocrinology
    • Psychiatry
    • Human Physiology

    Background:

    • Abnormal adrenocortical regulation, including excessive cortisol and loss of circadian rhythm, is observed in depression.
    • Norepinephrine (NE) is hypothesized to inhibit the hypothalamic-pituitary adrenal (HPA) axis, based on in vitro animal studies.

    Purpose of the Study:

    • To investigate the relationship between basal cortisol activity and HPA axis sensitivity to dexamethasone suppression.
    • To examine the correlation with basal noradrenergic activity, diurnal variation, and response to postural stimulation.
    • To explore the reciprocal interaction between cortisol and noradrenergic activity in humans.

    Main Methods:

    • Studied six normal human subjects.
    • Measured 24-hour urinary free cortisol for basal cortisol activity and dexamethasone suppression.

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  • Measured plasma NE for basal noradrenergic activity, diurnal variation, and response to postural stimulation.

    • Main Results:

    • Basal cortisol and dexamethasone suppression were inversely correlated with baseline NE response to stimulation.
    • NE response to stimulation after dexamethasone was inversely correlated with cortisol suppression.
    • Increased morning NE response post-dexamethasone inversely correlated with baseline and suppressed cortisol levels; diurnal variation in NE activity was observed.

    Conclusions:

    • Results support an inhibitory role for norepinephrine (NE) in regulating the HPA axis.
    • Findings suggest a reciprocal effect of cortisol on noradrenergic activity.
    • The study discusses implications for understanding adrenocortical dysregulation in depression.