α-Adrenergic Stimulation by Clonidine Increases Plasma Concentrations of Immunoreactive β-Endorphin in Rats

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Abstract
Peripheral administration of the .alpha.-adrenergic agonist clonidine (0.5 mg/kg s.c.) evoked a 2- to 3-fold rise (0.22 .+-. 0.03 to 0.59 .+-. 0.05 ng/ml) in plasma levels of .beta.-endorphin-like immunoreactivity (.beta.-END-LI) 15-30 min later in intact, but not hypophysectomized, rats. This rise in plasma .beta.-END-LI, which was dose dependent up to 0.5 mg/kg clonidine, appeared to be mediated by activation of .alpha.-adrenergic receptors, since pretreatment with the .alpha.-adrenergic antagonists yohimbine (1 mg/kg i.p.), phentolamine (1, 3 or 10 mg/kg, i.p.), or phenoxybenzamine (2 and 10 mg/kg i.p.) partially or fully blocked clonidine''s effect. The .beta.-adrenergic antagonist propranolol (1 and 5 mg/kg i.p.) did not modify the clonidine-induced increase in plasma .beta.-END-LI. Given alone, the adrenergic blocking drugs were generally without effect on plasma levels of .beta.-END-LI. Clonidine appeared to be acting on the brain (or pituitary), since the intracerebroventricular injection or phenoxybenzamine (20 .mu.g) blocked the drug-induced rise in plasma .beta.-END-LI. These data suggest an .alpha.-adrenergic mechanism influences the release of pituitary .beta.-END in the rat.
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