High tissue levels of
angiotensin II have been reported in the median eminence suggesting a possible role in the regulation of
adrenocorticotrophic hormone (
ACTH) secretion. To verify this hypothesis in man, the pituitary-adrenal axis response to hypoglycaemia was studied before and during
captopril treatment in eight male essential hypertensive patients (stage I WHO; aged 35-52 years). Plasma levels of
ACTH,
cortisol and
glucose were measured before and 60, 90 and 120 min after an intravenous bolus of
normal saline as placebo
an, 3 days later, after an intravenous bolus of rapidly acting
insulin (0.1 IU/kg
body weight).
Captopril treatment was then started and both placebo and hypoglycaemic tests were repeated 15 days thereafter. No changes in
ACTH,
cortisol or
glucose plasma levels were observed after acute
normal saline, either before or during
captopril administration. On the contrary, hypoglycaemia induced a sharp increase of
ACTH plasma before
captopril (from 27.7 +/- 11 to 131.30 +/- 26 pg/ml, P less than 0.01, 60 min after
insulin) but not during
angiotensin converting enzyme (ACE) inhibition (from 28.9 +/- 9 to 42.9 +/- 11 pg/ml, NS, at min 60 of the study). Our present data, showing a blunted
ACTH response to hypoglycaemia during ACE inhibition, suggest that circulating
angiotensin II may participate in the regulation of the release of the
ACTH, possibly by a stimulation of
angiotensin II receptors localized in the brain but outside the blood-brain barrier.