Differential effects of adrenergic agents on plasma levels of immunoreactive beta-endorphin and alpha-melanotropin in rats.

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) versus 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 less than 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 rises 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, whereas those of isoproterenol are beta-adrenergic. These studies extend earlier findings to indicate that clonidine is a selective activator of AL corticotroph secretion in vivo. On the other hand, other adrenergic agents such as norepinephrine, epinephrine, and isoproterenol appear to stimulate secretion from both corticotrophs as well as melanotrophs.