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Glucocorticoid-dependent hypertension.

F Mantero1, M Boscaro

  • 1Department of Medicine, Ospedale Garibaldi, University of Catania, Italy.

The Journal of Steroid Biochemistry and Molecular Biology
|October 1, 1992
PubMed
Summary
This summary is machine-generated.

Glucocorticoid excess causes hypertension in most Cushing's syndrome patients and 20% of those on GC treatment. This GC-induced hypertension, linked to cardiovascular risks, can be treated with GC antagonists.

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Area of Science:

  • Endocrinology
  • Cardiovascular Medicine
  • Pharmacology

Background:

  • Glucocorticoid (GC) excess, seen in Cushing's syndrome, is strongly linked to hypertension, affecting over 70% of patients.
  • Cardiovascular damage is prevalent in GC-induced hypertension and can occur even in normotensive individuals.
  • Excess mortality in Cushing's syndrome is largely attributed to cardiovascular disease, highlighting the systemic impact of GC excess.

Purpose of the Study:

  • To investigate the association between glucocorticoid excess and hypertension.
  • To explore the mechanisms underlying GC-induced hypertension and its cardiovascular consequences.
  • To assess the efficacy of GC antagonists in managing GC-related hypertension.

Main Methods:

  • Analysis of hypertension prevalence in Cushing's syndrome patients (n=130).
  • Examination of cardiovascular damage in hypertensive and normotensive GC-affected individuals.
  • Experimental induction of hypertension using oral cortisol and assessment of vascular responsiveness.

Main Results:

  • Hypertension is prevalent in Cushing's syndrome (89/130 patients) and in 20% of patients on oral GC therapy, independent of disease subtype or duration.
  • GC-induced hypertension is unresponsive to spironolactone but sensitive to GC antagonists like RU486.
  • Experimentally, cortisol administration increased cardiac output and forearm vascular responsiveness, suggesting local vascular mechanisms contribute to hypertension.

Conclusions:

  • Glucocorticoid excess is a significant cause of hypertension with substantial cardiovascular implications.
  • The hypertension associated with GC excess appears to involve altered vascular responsiveness, potentially mediated by local mechanisms.
  • Glucocorticoid antagonists represent a potential therapeutic strategy for managing GC-induced hypertension.