Differential Effects of Adrenergic Agents on Plasma Levels of Immunoreactive -Endorphin and -Melanotropin in Rats

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Abstract
Parallel measurements of plasma .alpha.-melanotropin-like immunoreactivity (.alpha.-MSH-LI) and .beta.-endorphin-like immunoreactivity (.beta.-END-LI) were used to examine the differential adrenergic control of .beta.-END secretion from the anterior lobe (AL) vs. the intermediate lobe (IL) of the rat pituitary gland in vivo. Changes in plasma .alpha.-MSH-LI levels after treatment with various adrenergic agents served as an index of the secretion of the peptides by the IL. Secretion of .beta.-END-LI from the AL in vivo was evaluated using the selective inhibitory effects of dexamethasone on AL release. Inhibition of glucocorticoid synthesis by metyrapone or activation of .alpha.-adrenoceptors by clonidine increased (P < 0.05) plasma levels of .beta.-END-LI while plasma levels of .alpha.-MSH-LI were not affected by either treatment. By contrast, peripherally administered isoproterenol, norepinephrine or epinephrine, each increased plasma levels of .alpha.-MSH-LI together with .beta.-END-LI in a dose-dependent manner. The synthetic glucocorticoid, dexamethasone, significantly attenuated the rise in plasma .beta.-END-LI induced by norepinephrine and epinephrine but did not affect the rise in .alpha.-MSH-LI. The isoproterenol-induced rise in .beta.-END-LI and .alpha.-MSH-LI were inhibited by the .beta.-adrenergic blocker propranolol. By contrast, the .alpha.-adrenergic blockers, phentolamine or prazosin, reversed the effect of epinephrine on both peptides while propranolol had no significant effect. The effects of epinephrine, therefore, appear to be .alpha.-adrenergic; those of isoproterenol are .beta.-adrenergic. Clonidine is a selective activator of AL corticotroph secretion in vivo. Other adrenergic agents such as norepinephrine, epinephrine and isoproterenol appear to stimulate secretion from both corticotrophs as well as melanotrophs.