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      Adrenocorticotropin, Prolactin and Beta-Endorphin Stimulatory Actions of Alpha-2-Adrenoceptor Antagonists

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          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 α<sub>2</sub>-antagonists. The pretreatment of 1 mg/kg s.c. dexamethasone for 4 days effectively prevented the stimulatory effect of α<sub>2</sub>-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 α<sub>2</sub>-antagonists stimulate ACTH secretion by a cortico-steroid-sensitive mechanism which is located centrally. In contrast, α<sub>2</sub>-antagonists affect PRL and βE secretion via a corticosteroid-insensitive mechanism located at the periphery, possible within the pituitary gland.

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          Author and article information

          S. Karger AG
          09 April 2008
          : 61
          : 2
          : 152-158
          aInstitute of Experimental Medicine, Hungarian Academy of Sciences, Budapest, Hungary; bDepartment of Physiology and Biophysics, Georgetown University School of Medicine, Washington, D.C., USA
          126835 Neuroendocrinology 1995;61:152–158
          © 1995 S. Karger AG, Basel

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          Page count
          Pages: 7
          Corticotropin and Proopiomelanocortin Regulation


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