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Cortisol and hypertension

J J Kelly1, G Mangos, P M Williamson

  • 1Department of Medicine, St George Hospital, University of New South Wales, Sydney, Australia. jkelly@s056.aone.net.au

Clinical and Experimental Pharmacology & Physiology. Supplement
|November 11, 1998
PubMed
Summary
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Cortisol, a stress hormone, can cause hypertension (high blood pressure) in humans. This effect is not primarily due to sodium retention or increased sympathetic activity, but may involve the nitric oxide system.

Area of Science:

  • Endocrinology
  • Cardiovascular Physiology

Background:

  • Adrenocorticotropic hormone (ACTH) infusion in humans mimics hypertensive effects with cortisol.
  • Oral cortisol administration leads to dose-dependent increases in blood pressure, with significant effects observed within 24 hours.

Purpose of the Study:

  • To investigate the mechanisms underlying cortisol-induced hypertension.
  • To determine the role of sodium retention, sympathetic activity, and the nitric oxide system in cortisol-mediated blood pressure elevation.

Main Methods:

  • Administration of oral cortisol to human subjects at doses of 80-200 mg/day.
  • Co-administration of cortisol with the mineralocorticoid receptor antagonist spironolactone.
  • Measurement of direct and indirect sympathetic activity.
  • Assessment of the nitric oxide system's involvement.

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Main Results:

  • Cortisol administration caused dose-dependent increases in systolic blood pressure (up to 15 mmHg).
  • Cortisol-induced hypertension was associated with sodium retention and volume expansion, but spironolactone did not prevent hypertension, indicating sodium retention is not the primary mechanism.
  • Sympathetic activity remained unchanged or was suppressed during cortisol administration.
  • Preliminary evidence suggests suppression of the nitric oxide system may contribute to cortisol-induced hypertension.

Conclusions:

  • Cortisol-induced hypertension in humans is not primarily mediated by increased sympathetic tone or sodium retention.
  • Suppression of the nitric oxide system is a potential mechanism for cortisol-induced hypertension.
  • These findings have implications for understanding hypertension in conditions like Cushing's syndrome, apparent mineralocorticoid excess, liquorice abuse, and potentially essential hypertension.