Cortisol and hypertension

Clin Exp Pharmacol Physiol Suppl. 1998 Nov;25:S51-6. doi: 10.1111/j.1440-1681.1998.tb02301.x.

Abstract

1. In humans, the hypertensive effects of adrenocorticotropic hormone (ACTH) infusion are reproduced by intravenous or oral cortisol. Oral cortisol increases blood pressure in a dose-dependent fashion. At a dose of 80-200 mg/day, the peak increases in systolic pressure are of the order of 15 mmHg. Increases in blood pressure are apparent within 24 h. 2. Cortisol-induced hypertension is accompanied by a significant sodium retention and volume expansion. Co-administration of the type I (mineralocorticoid) receptor antagonist spironolactone does not prevent the onset of cortisol-induced hypertension. Thus, sodium retention is not the primary mechanism of cortisol-induced hypertension. 3. Direct and indirect measures of sympathetic activity are unchanged or suppressed during cortisol administration, suggesting that cortisol-induced hypertension is not mediated by increased sympathetic tone. 4. Preliminary evidence in humans suggests that suppression of the nitric oxide system may play a role in cortisol-induced hypertension. 5. These potential mechanisms of cortisol action may be relevant in a number of clinical contexts, including Cushing's syndrome, apparent mineralocorticoid excess, the hypertension of liquorice abuse and chronic renal failure. There is also preliminary evidence suggesting a role for cortisol in essential hypertension.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Adrenocorticotropic Hormone / pharmacology
  • Animals
  • Cardiac Output / drug effects
  • Cushing Syndrome / etiology
  • Epinephrine / metabolism
  • Humans
  • Hydrocortisone / pharmacology*
  • Hypertension / chemically induced*
  • Muscle, Smooth, Vascular / physiology
  • Norepinephrine / metabolism
  • Sodium / metabolism

Substances

  • Adrenocorticotropic Hormone
  • Sodium
  • Hydrocortisone
  • Norepinephrine
  • Epinephrine