Abstract

Publisher Summary This chapter discusses antimitotic actions of dopaminergic drugs on human pituitary tumors. Normal prolactin (PRL) secretion by the pituitary gland is under the tonic inhibitory control of the hypothalamus. It is generally accepted that the most important and probably only hypothalamic PRL release-inhibiting factor is dopamine, which is synthesized in the tuberoinfundibular neurons of the hypothalamus, secreted into the hypothalamo-hypophyseal portal system, and transported to the anterior pituitary gland where it directly inhibits the secretion of PRL by lactotropic cells. The primary action of dopamine and its agonists on the pituitary lactotroph is to inhibit the secretion of PRL. The time-dependent dose relationship and duration of action of this amine have been extensively studied with the aid of the perifused pituitary cell column. An increase in hormone secretion is usually accompanied by increased proliferation of the respective endocrine gland cells, whereas diminution of secretion is usually associated with a decrease of cell proliferation. There is also evidence indicating that the secretory function and cell proliferation of PRL-secreting cells are closely related. Suppression of PRL secretion by dopamine agonists for a long duration, leads to attenuation of cell metabolism and mitotic processes. The antimitotic action of dopaminergic drugs on human PRL-secreting pituitary tumors are confined to a complete cessation of mitosis and a partial, reversible emptying of the tumor cell with no important cytotoxic effect.

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