Adrenocorticotropin, prolactin and beta-endorphin stimulatory actions of alpha-2-adrenoceptor antagonists

Do T. Kiem, István Barna, James I. Koenig, Gabor Makar

Research output: Contribution to journalArticle

13 Citations (Scopus)


We studied the effect of glucocorticoid pretreatment, mediobasal hypothalamus lesion (MBHL) and the interaction between clonidine and yohimbine in male Wistar rats to elucidate the sites and/or mechanisms of endocrine actions of α2-antagonists. The pretreatment of 1 mg/kg s.c. dexamethasone for 4 days effectively prevented the stimulatory effect of α2-antagonists yohimbine (5 mg/kg i.p.) and CH-38083 (1 mg/kg i.p.) on adrenocorticotropin (ACTH) secretion, while the action of these antagonists on prolactin (PRL) and β-endorphin (βE) remained unchanged. The central (i.c.v.) pretreatment of 5 µg/rat clonidine failed to antagonize the prolactin (PRL) and βE releasing effect of yohimbine. However, it inhibited the yohimbine-induced ACTH secretion. MBHL resulted in a significant enhancement in basal plasma PRL and β-endorphin (βE) levels. But basal plasma ACTH levels have not been changed. Yohimbine failed to stimulate ACTH secretion in MBH-lesions rats, while PRL and βE response to the yohimbine was maintained in these animals. This study confirms that the α2-antagonists stimulate ACTH secretion by a cortico-steroid-sensitive mechanism which is located centrally. In contrast, α2-antagonists affect PRL and βE secretion via a corticosteroid-insensitive mechanism located at the periphery, possible within the pituitary gland.

Original languageEnglish
Pages (from-to)152-158
Number of pages7
Issue number2
Publication statusPublished - Jan 1 1995


  • Adrenal steroids
  • Beta-endorphin
  • Catecholamine receptors
  • Corticotropin
  • Prolactin

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Endocrinology
  • Endocrine and Autonomic Systems
  • Cellular and Molecular Neuroscience

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