Pituitary—adrenocortical Function in Patients During Treatment With the Angiotensin‐converting Enzyme Inhibitor Captopril

Abstract

To study effects on pituitary-adrenocortical activity of a sustained block of angiotensin II formation, six 'drug-resistant' patients with essential hypertension were studied before and during treatment with an inhibitor of the angiotensin-converting enzyme (Captopril, SQ 14,225). The drug was given in increasing doses (100-400 mg/day) for 2 weeks whilst patients received a moderately restricted sodium intake (60-80 mmol/day). Immunoreactive ACTH, cortisol, aldosterone, plasma renin activity (PRA) and the activity of the angiotensin-converting enzyme (ACE) were measured in blood samples drawn at 0800-0900 h. Urinary excretion of cortisol and aldosterone were measured in 24-h urine collections. Further information on pituitary-adreno-cortical function was obtained by measuring serial plasma corticosteroid levels after submaximal stimulation with a synthetic ACTH preparation. ACTH and cortisol did not change an observation which does not support the hypothesis that glucocorticoid activity is influenced by a decrease in plasma angiotensin II concentrations.

The Effect of Angiotensin-Converting Enzyme Inhibition on ACTH Response to Corticotropin-Releasing Hormone (CRH) in Normal Men

“…The data from the literature concerning the captopril effect on ACTH release are controversial. It has been reported previously that two weeks captopril treatment does not change ACTH and Cortisol levels in patients with essential hypertension (Angeli, Bisbocci, Orlandi, Paccoti, Tabasso, Tamagnone and Lavezzaro 1981). Others showed unchanged basal levels, but blunted ACTH and Cortisol responses to hypoglycemia after captopril treatment in hypertensive patients {Magna, Dessy-Fulgheri, Masala, Mededdu, Rovasio, Glorioso and Rappelli 1989).…”

Role of the renin-angiotensin system in the control of vasopressin and ACTH secretion during the development of renal hypertension in dogs.

“…Treatment with captopril caused a reduction in plasma cortisol concentration in the patients with high renin but not in the normal or low renin groups. Angeli et al 27 also measured plasma cortisol concentration in six patients with essential hypertension. Analysis of their data reveals a significant correlation between PRA and plasma cortisol concentration (r = 0.91, p < 0.01).…”