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Corticosteroid hypertension

J W Funder1

  • 1Baker Medical Research Institute, Prahran, Victoria, Australia.

Current Opinion in Nephrology and Hypertension
|September 1, 1995
PubMed
Summary
This summary is machine-generated.

Researchers identified mutations in the 11 beta-hydroxysteroid dehydrogenase enzyme, a key factor in apparent mineralocorticoid excess syndrome. This finding advances understanding of single-gene causes of hypertension and aldosterone

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Area of Science:

  • Endocrinology
  • Genetics
  • Cardiovascular Medicine

Background:

  • Corticosteroid hypertension research has focused on the enzyme 11 beta-hydroxysteroid dehydrogenase.
  • Apparent mineralocorticoid excess syndrome is now the third single-gene cause of human hypertension identified.
  • Previous discoveries include glucocorticoid remediable aldosteronism (1992) and Liddle's syndrome (1994).

Purpose of the Study:

  • To investigate the role of 11 beta-hydroxysteroid dehydrogenase mutations in apparent mineralocorticoid excess.
  • To further elucidate the genetic underpinnings of mineralocorticoid hypertension.

Main Methods:

  • Cloning of the 11 beta-hydroxysteroid dehydrogenase enzyme.
  • Analysis of mutations and deletions in the enzyme's coding sequence.

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Main Results:

  • Demonstration of various mutations/deletions in 11 beta-hydroxysteroid dehydrogenase in apparent mineralocorticoid excess.
  • These genetic defects contribute to inappropriate aldosterone action and sodium retention.

Conclusions:

  • Apparent mineralocorticoid excess, Liddle's syndrome, and glucocorticoid remediable aldosteronism highlight the role of aldosterone-salt imbalance in hypertension.
  • Further research is needed to explore mechanisms of hypertension related to glucocorticoid receptor occupancy.