Blunted adrenocorticotrophic hormone release during captopril treatment.

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.