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CORTISOL AND HYPERTENSION
Author(s) -
Kelly JJ,
Mangos G.,
Williamson PM,
Whitworth JA
Publication year - 1998
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.1998.tb02301.x
Subject(s) - medicine , cardiology , endocrinology
SUMMARY 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 15mmHg. 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.