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

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Summary

The role of alpha2-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.

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Słowinska-Srzednicka, J., Zgliczynski, S., Soszynski, P. et al. Effect of clonidine on beta-endorphin, ACTH and cortisol secretion in essential hypertension and obesity. Eur J Clin Pharmacol 35, 115–121 (1988). https://doi.org/10.1007/BF00609239

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  • DOI: https://doi.org/10.1007/BF00609239

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