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Insights Into Glucocorticoid-Associated Hypertension.

A S Brem1

  • 1Division of Pediatric Nephrology, Rhode Island Hospital, and Brown University School of Medicine, Providence, RI 02903, USA. andrew_brem@brown.edu

American Journal of Kidney Diseases : the Official Journal of the National Kidney Foundation
|January 3, 2001
PubMed
Summary

Excess glucocorticoids contribute to hypertension by affecting blood pressure regulation sites. Enzymes like 11-beta-hydroxysteroid dehydrogenase (11-beta-HSD) metabolize these steroids, influencing sodium transport and vascular responses.

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Area of Science:

  • Endocrinology
  • Nephrology
  • Cardiovascular Physiology

Background:

  • The link between excess glucocorticoids and hypertension is established but not fully understood.
  • Glucocorticoids impact multiple blood pressure regulation sites.
  • 11-beta-hydroxysteroid dehydrogenase (11-beta-HSD) enzymes metabolize glucocorticoids, controlling receptor access.

Purpose of the Study:

  • To elucidate the mechanisms by which glucocorticoids influence blood pressure regulation.
  • To investigate the role of 11-beta-HSD in glucocorticoid-mediated effects on sodium transport and vascular resistance.

Main Methods:

  • Review of clinical observations and laboratory studies.
  • Analysis of glucocorticoid effects on renal tubular sodium transport.
  • Examination of glucocorticoid actions on vascular tissue responses to vasoconstrictors.

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Main Results:

  • Inhibition of 11-beta-HSD enhances glucocorticoid-induced sodium transport in the kidney.
  • Glucocorticoids increase Na(+), K(+) ATPase and Na(+)-H(+) exchanger expression in proximal tubules, potentiating angiotensin II effects.
  • Glucocorticoids can bind to mineralocorticoid receptors in distal renal segments.
  • In vascular tissue, glucocorticoids upregulate vasoconstrictor receptors and downregulate vasodilator effects, magnifying responses to vasoconstrictors.

Conclusions:

  • Glucocorticoids alter both circulating volume and vascular resistance, contributing to hypertension.
  • 11-beta-HSD plays a critical role in modulating glucocorticoid action in various tissues.
  • Understanding these mechanisms is key to managing glucocorticoid-induced hypertension.