Dopamine or its agonists inhibit PRL release from the anterior pituitary both in vivo and in vitro, while specific dopaminergic antagonists can reverse this inhibition. The direct measurement of dopamine in portal blood and dopamine receptors in the anterior pituitary of the rat, sheep, and steer with radioligand-binding assays supports the hypothesis that dopamine is a PRL inhibitory factor. In the present study, [3H]spiperone (a dopamine antagonist) bound to an apparent single class of high affinity sites in human anterior pituitaries as well as in human PRL-secreting pituitary adenomas. Neither the dissociation constant [Kd = 2.2 ± 0.7 and 3.1 ± 1.4 nM, respectively (mean ± SEM)] nor the site numbers per PRL content were different in these two tissues. However, if the site numbers were expressed per mg protein, there were significantly more sites in the PRL-secreting pituitary adenomas (707 ±113 fm/mg protein; n = 5) than in the control anterior pituitaries (141 ± 22 fm/mg protein; n = 7). This may be due to an increased density of mammotrophs and, thus, an increased number of binding sites in the adenomas. The development of PRL-secreting pituitary adenomas is probably not due to the absence of dopamine receptors or a decrease in their affinity for [3H]spiperone. There was undetectable binding in two of four experiments with GH-secreting adenomas and in two with ACTHproducing adenomas. In the other two experiments with GHsecreting adenomas, site numbers similar to the control anterior pituitaries were observed.
ASJC Scopus subject areas
- Endocrinology, Diabetes and Metabolism
- Clinical Biochemistry
- Biochemistry, medical