Effect of clonidine on beta-endorphin, ACTH and cortisol secretion in essential hypertension and obesity

Abstract

The role of alpha 2-adrenoceptor stimulation by clonidine on the secretion of beta-endorphin, ACTH, and cortisol in essential hypertension and obesity was studied in 45 subjects: 15 non-obese hypertensives, 10 obese hypertensives, 11 obese normotensives, and 9 healthy subjects. The circadian rhythm of plasma beta-endorphin, ACTH, and cortisol was determined after placebo and after three days on clonidine 0.45 mg daily. Clonidine lowered the blood pressure and blood ACTH and cortisol levels in all the subjects. A significant decrease in beta-endorphin after clonidine occurred in the healthy subjects. In obese normotensives basal beta-endorphin concentrations were significantly higher than in healthy subjects and did not change after clonidine. In about 50% of non-obese and obese hypertensives a significant increase in beta-endorphin secretion after clonidine was noted (responders). In the subgroup of non-obese hypertensive responders no circadian rhythm of beta-endorphin was observed. The results suggest that adrenergic regulation of beta-endorphin secretion is altered in obesity and in certain patients with essential hypertension.

The Hypothalamic‐Pituitary‐Adrenal Axis in Obesity

“…However, Facchineni et al found that dexamethasone failed to suppress hyperendorphinemia in obese patients (35,36). Administration of clonidine for 3 days to obese normotensive subjects was found to reduce cortisol and ACTH but did not alter elevated Bendorphin levels (108).…”