Abstract
Abstract
Parallel measurements of plasma α-melanotropin-like immunoreactivity (α-MSH-LI) and β-endorphin-like immunoreactivity (β-END-LI) were used to examine the differential adrenergic control of β-END secretion from the anterior lobe (AL) versus the intermediate lobe (IL) of the rat pituitary gland in vivo. Changes in plasma α-MSH-LI levels after treatment with various adrenergic agents served as an index of the secretion of the peptides by the IL. Secretion of β-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 α-adrenoceptors by clonidine increased (P < 0.05) plasma levels of β-END-LI while plasma levels of α-MSH-LI were not affected by either treatment. By contrast, peripherally administered isoproterenol, norepinephrine or epinephrine, each increased plasma levels of α-MSH-LI together with β-END-LI in a dose-dependent manner. The synthetic glucocorticoid, dexamethasone, significantly attenuated the rise in plasma β-END-LI induced by norepinephrine and epinephrine but did not affect the rise in α-MSH-LI. The isoproterenol-induced rises in β-END-LI and α-MSH-LI were inhibited by the β-adrenergic blocker propranolol. By contrast, the α-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 a-adrenergic, whereas those of isoproterenol are β-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.
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