Abstract：
:An in vitro perifusion system was used to investigate the effects of GnRH stimulation on LH, ACTH, and immunoreactive beta-endorphin (i beta-END) release from ovariectomized (1 week) rat anterior hemipituitaries. Either 0, 8 or 80 nM GnRH was administered as a 15 min pulse followed 30 min later by a prolonged 45 min infusion. Both 8 and 80 nM GnRH induced comparable LH release in response to the 15 min as well as the 45 min GnRH stimulation. The initial 15 min exposure to either 8 or 80 nM GnRH did not induce significant changes in ACTH or i beta-END release. In contrast, the subsequent 45 min exposure to 8 nM GnRH induced a significant (p less than 0.01) increase in ACTH release, and the 45 min exposure to 80 nM GnRH induced a significant (p less than 0.01) increase in ACTH as well as i beta-END release. Equimolar (i.e. 8 or 80 nM) GnRH receptor antagonist (ANT) blocked the stimulatory effects of GnRH in all cases. These results demonstrate that GnRH can stimulate not only LH but also ACTH and i beta-END release from ovariectomized rat anterior hemipituitaries in vitro, apparently by a GnRH receptor mediated mechanism independent of actual LH release. Although the time course of these responses appears to be consistent with the hypothesis that GnRH-stimulated gonadotropes release paracrine factor(s) which stimulate corticotrope activity, the mechanism of these responses remains to be determined.
journal_name
Life Scijournal_title
Life sciencesauthors
Gambacciani M,Yen SS,Rasmussen DDdoi
10.1016/0024-3205(88)90175-0subject
Has Abstractpub_date
1988-01-01 00:00:00pages
755-60issue
9eissn
0024-3205issn
1879-0631pii
0024-3205(88)90175-0journal_volume
43pub_type
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