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  • Title: [Mechanism of beta-endorphin release regulation--evaluation using dispersed cells of the pituitary intermediate lobe].
    Author: Furuki Y.
    Journal: Nihon Sanka Fujinka Gakkai Zasshi; 1983 Sep; 35(9):1604-10. PubMed ID: 6311922.
    Abstract:
    The intermediate lobe of the rat pituitary gland is a homogeneous population of cells synthesizing and secreting various peptides related to ACTH and lipotropin derived from a common glycoprotein precursor, pro-opiocortin. The release mechanism of beta-endorphin from the pituitary gland has been reported by a few investigators, but the precise mechanism is still unknown. The receptors for a catecholamine present in the intact intermediate lobe of the rat pituitary gland remain functional on the enzymatically dispersed cells which secrete beta-endorphin-like immunoreactivity (beta-EPLI) and synthesize adenosine-3',5'-monophosphate (cAMP). Stimulation of beta-adrenoceptor with 1-isoproterenol enhances the synthesis of cAMP and accelerates the rate of beta-EPLI release. The ability of beta-adrenergic agonists to enhance the synthesis of cAMP appears to be causally related to the physiological response to beta-adrenergic agonists (i.e. enhanced beta-EPLI release). Phosphodiesterase inhibitors (theophylline, 3-isobutyl-1-methyl xanthine), cAMP analogs (dibutyryl-cAMP, 8-bromo-cAMP) and cholera toxin also increase beta-EPLI release. These findings suggest that cAMP may participate in this beta-EPLI release process. Furthermore, dopamine inhibits basal beta-EPLI release and also diminishes l-isoproterenol stimulated beta-EPLI release.
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