Abstract

Haloperidol (0.03–3 mg/kg) dose-dependently increased the plasma concentrations of immunorcactivc β-endorphin (ir-β-END) without changing the concentrations of ir-β-END in the adenohypophysis or the neurointermediate pituitary of rats. Elevated levels of ir-β-END in plasma were also found after chronic treatment with haloperidol (1mg/kg per day) for 3 weeks. The long-term treatment, however, caused a selective increase (60%) of the ir-β-END concentrations in the neurointermediate pituitary without changing that in the adenohypophysis. Significantly elevated levels of ir-β-END were also found in the hypothalamus and the septum. Gelchromatographic separation of the plasma components reacting with the β-endorphin antiserum revealed that both the acute and chronic haloperidol treatment increased the plasma concentrations of immunoreactive material with the molecular size of β-endorphin and β-lipotropin. This indicates that, at least, part of ir-β-END released by halopcridol into plasma is of adcnohypophyscal origin, since no material with the molecular size of β-lipotropin has been found in the neurointermediate pituitary.

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