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- Title
Effects of Gonadotropin-Releasing Hormone and Its Agonists on Prolactin Secretion from Normal and Tumorous Pituitary Cells.
- Authors
Lamberts, Steven W.J.; Uitterlinden, Piet; Reubi, Jean-Claude; de Jong, Frank H.
- Abstract
Previous studies on the effect of gonadotropin-releasing hormone (LHRH) agonist on prolactin (PRL) secretion from normal and tumorous pituitary cells have not been conclusive as to the mechanism of action of these agonists. In this study the short-term administration of a LHRH agonist did not affect circulating PRL levels, but depleted the PRL content of the pituitary gland by 24, 49 and 73% after 2, 3 and 4 days, respectively, in normal female rats and by 75% after 4 days in normal male rats. This effect of the agonist could not be attributed to changes in the sex steroid environment: although plasma 17β-estradiol concentrations were significantly suppressed in female rats, circulating testosterone levels had not changed yet in the male rats. Interestingly, the pituitary luteinizing hormone (LH) content was depleted already from day 2 of LHRH agonist administration onwards, while the follicle-stimulating hormone (FSH) content of the pituitary glands had not changed even after 4 days. Culture studies with pituitary cells from normal adult male and female rats for 4-7 days did not reveal a direct effect of synthetic LHRH or an agonist on PRL release. Chronic systemic administration of a LHRHagonist greatly inhibited the growth of the transplantable PRL-secreting rat pituitary tumor 7315a in female rats, while circulating PRL levels were also suppressed. However, no direct effect of the LHRH agonist was observed on PRL release from a tumor cell clone, derived from the 7315a tumor, and no LHRH-binding sites were detectable on the tumor. These studies support the hypothesis of an indirect effect of LHRH (agonists) on PRL secretion via paracrine secretions of the gonadotrophs. This paracrine factor might originate from the LH-secreting cells, as depletion of the LH- and PRL-secreting cells occurs when the FSH content of the pituitary is not affected. In the model of the transplantable PRL-secreting rat pituitary tumor 7315a, LHRH agonists apparently inhibit tumor growth via an indirect mechanism involving chemical castration, because no LHRH-binding sites or a direct effect on PRL secretion could be shown Copyright © 1989 S. Karger AG, Basel
- Publication
Neuroendocrinology, 1989, Vol 49, Issue 2, p157
- ISSN
0028-3835
- Publication type
Article
- DOI
10.1159/000125108