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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.
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.
Abstract:
Cushing's syndrome of glucocorticoid excess is named after the eminent Boston neurosurgeon Harvey W. Cushing (1869-1939). The recognition that glucocorticoid excess produces hypertension led to examination of the role of cortisol in essential hypertension, but it is only over the last decade that evidence has emerged to support the concept. Despite the widespread assumption that cortisol raises blood pressure as a consequence of renal sodium retention, there are few data consistent with the notion. Although it has a plethora of actions on brain, heart and blood vessels, kidney, and body fluid compartments, precisely how cortisol elevates blood pressure is unclear. Candidate mechanisms currently being examined include inhibition of the vasodilator nitric oxide system and increases in vasoconstrictor erythropoietin concentration.