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Corticosteroids decrease glomerular angiotensin receptors.

J G Douglas

    The American Journal of Physiology
    |March 1, 1987
    PubMed
    Summary
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    Corticosteroids, like aldosterone and dexamethasone, downregulate glomerular Angiotensin II receptors. This finding suggests a role for corticosteroids in regulating kidney function and blood pressure.

    Area of Science:

    • Nephrology
    • Endocrinology
    • Molecular Biology

    Background:

    • Glomerular Angiotensin II (ANG II) receptors are modulated by sodium balance, likely via circulating ANG II.
    • Aldosterone levels often parallel ANG II changes, suggesting a potential role for aldosterone in receptor regulation.

    Purpose of the Study:

    • To investigate the hypothesis that aldosterone modulates glomerular ANG II receptors.
    • To determine the mineralocorticoid specificity of this effect using dexamethasone and spironolactone.

    Main Methods:

    • Short-term infusions of physiological aldosterone and dexamethasone in rats.
    • Measurement of glomerular ANG II receptor density and affinity.
    • Assessment of serum potassium, urinary Na/K ratio, and adrenal receptor density.

    Related Experiment Videos

  • Evaluation of spironolactone's effect on aldosterone-induced changes.

    • Main Results:

    • Aldosterone infusion decreased glomerular ANG II receptor density by 33% and 45% at two different rates.
    • Dexamethasone also caused similar downregulation of glomerular ANG II receptors.
    • Spironolactone blocked the effect of aldosterone, indicating mineralocorticoid receptor mediation.
    • No changes in ANG II receptor affinity or adrenal receptor density were observed.

    Conclusions:

    • Corticosteroids, including aldosterone and glucocorticoids, can downregulate glomerular ANG II receptors.
    • This downregulation may impact glomerular hemodynamics in conditions like mineralocorticoid and glucocorticoid-induced hypertension.