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Cushing, cortisol, and cardiovascular disease

J A Whitworth1, G J Mangos, J J Kelly

  • 1John Curtin School of Medical Research, The Australian National University, Canberra, ACT.

Hypertension (Dallas, Tex. : 1979)
|November 18, 2000
PubMed

Insights

Glucocorticoid excess, or Cushing's syndrome, is linked to hypertension. Research is exploring how cortisol raises blood pressure, moving beyond sodium retention theories.

Area of Science:

  • Endocrinology
  • Nephrology
  • Cardiovascular Medicine

Background:

  • Cushing's syndrome is characterized by glucocorticoid excess.
  • Glucocorticoid excess is recognized as a cause of hypertension.
  • The precise mechanisms by which cortisol elevates blood pressure are not fully understood.

Purpose of the Study:

  • To examine the role of cortisol in essential hypertension.
  • To investigate the mechanisms underlying cortisol-induced hypertension.
  • To evaluate the evidence supporting cortisol's role in elevated blood pressure.

Main Methods:

  • Review of existing literature on glucocorticoid excess and hypertension.
  • Analysis of data on cortisol's actions on various organ systems.
  • Investigation of candidate mechanisms, including nitric oxide inhibition and erythropoietin changes.

Main Results:

  • Evidence supporting cortisol's role in essential hypertension has emerged recently.
  • The assumption that cortisol raises blood pressure solely via renal sodium retention lacks substantial data.
  • Potential mechanisms involve inhibition of the nitric oxide system and increased erythropoietin concentration.

Conclusions:

  • Cortisol's role in hypertension is increasingly recognized.
  • The exact pathways of cortisol-mediated blood pressure elevation require further elucidation.
  • Inhibition of vasodilation and augmentation of vasoconstriction are potential mechanisms.

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