Release of Newly Synthesized Dopamine into the Hypophysial Portal Vasculature of the Rat*

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Abstract
The concentrations of dopamine and norepinephrine in pituitary stalk and arterial plasma from rats were determined after the administration of pharmacological agents known to influence neurotransmission in dopaminergic neurons of the brain and to alter the release of PRL from the anterior pituitarygland. The concentrations of dopamine and norepinephrine in pituitary stalk plasma from male rats were markedly elevated after an infusion of rf-amphetamine (5.0 mg/kg, iv). In addition, the arterial plasma concentrations of norepinephrine, but not dopamine, were also elevated in these animals. In male rats which had been pretreated with α-methyltyrosine (50 mg/kg, iv), amphetamine was ineffective in elevating the concentration of dopamine in stalk plasma but was effective in increasing the concentration of norepinephrine in pituitary stalk and arterial plasma. Although reserpine treatment led to a 95% reduction in the dopamine content of the median eminence and a reduction in catecholamine concentrations in stalk plasma, the release of dopamine into pituitary stalk blood in reserpine-treated rats was still enhanced by amphetamine. Amphetamine-induced increases in stalk and arterial plasma concentrations of norepinephrine were largely prevented by reserpine pretreatment. Administration of α-methyltyrosine (50 mg/kg, iv) to pregnant rats resulted in an 80% reduction in the pituitary stalk plasma concentrations of dopamine but had no effect on norepinephrine concentrations in stalk plasma. These results are consi stent with the hypothesis that dopamine in pituitary stalk blood reflects the preferential release of dopamine from a small, newly synthesized pool of this neurotransmitter and that amphetamine acts to enhance the release of this newly synthesized dopamine. Furthermore, the abilities of α-methyltyrosine and amphetamine to inhibit and stimulate, respectively, the release of dopamine into pituitary portal blood may be the mechanisms by which these drugs alter the release of PRL from the pituitary gland.