1. In humans, the hypertensive effects of adrenocorticotropic hormone
(ACTH) infusion are reproduced by intravenous or oral cortisol. Oral c
ortisol increases blood pressure in a dose-dependent fashion. At a dos
e 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 so
dium retention and volume expansion. Go-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 suppre
ssed during cortisol administration, suggesting that cortisol-induced
hypertension is not mediated by increased sympathetic tone. 4. Prelimi
nary evidence in humans suggests that suppression of the nitric oxide
system may play a role in cortisol-induced hypertension. 5. These pote
ntial mechanisms of cortisol action may be relevant in a number of cli
nical contexts, including Gushing's syndrome, apparent mineralocortico
id excess, the hypertension of liquorice abuse and chronic renal failu
re. There is also preliminary evidence suggesting a role for cortisol
in essential hypertension.