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The proliferation and tumor transformation of AP cells is controled by
many molecular regulators, such as neurotransmitters, neuromodulators,
and neurohormones. MacLeod and Lehmeyer (1974) were the first to unequivocally
indicate that dopamine acts at the pituitary level. By the early and mid-1970s,
it had become clear that dopamine is the key transmitter in the inhibition
of prolactin secretion. Abnormalities of dopaminergic neurons that release
dopamine (DA), a potent physiological inhibitor of prolactin secretion,
cell division, and tumor transformation, can accompany the development
of pituitary tumors (Gottschall and Meites, 1986). The direct effect of
inhibitory and stimulatory hypothalamic factors on the lactotrophs are
modified by "peripheral" hormones that reach the anterior pituitary gland
via the systemic circulation. Of these, estrogens and thyroid hormones
occupy an important position in the influence on cell division of AP cells,
particularly lactotrophs (Schreiber, Pribyl, Rohácová, 1970,
Dušková and Schreiber, 1989). Experimental hypertrophy of the rat
adenohypophysis after administration of the estrogens was first described
by Selye et al (Selye, Collip, Thomson, 1935). Koga et al (Koga, Nakao,
Sato, 1992) and Zhou-Li et al (Zhou-li, Joly-Pharaboz, Bouillard, 1991)
demonstrated under in vitro conditions that in cell cultures the pituitary
tumor-cell proliferation is stimulated by estrogens and thyroid hormones.
In vivo, however, Schreiber et al. (Schreiber, Pribyl, Rohácová,
1979., Schreiber. 1979) and Duškova and Schreiber (1989) have shown that
this growth reaction is potentiated by dopaminergic antagonists and inhibited
by dopaminergic agonists and thyroid hormones. Recently Adams et al. (1994),
documented significant pituitary hyperplasia associated with primary hypothyroidism.
Velardo et al. (1994) confirmed that thyroxine treatment of hypothyroid
patients depressed higher plasma levels of prolactin and modified the enhanced
response to TRH.
On the basis of these results we assume that central catecholaminergic
systems appear to participate in the interactions between thyroid hormones
and estrogens in the regulation of AP hyperplasia.
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