Abstract:
:The systemic administration of neurotensin (NT) dose-dependently increased plasma adrenocorticotropin (ACTH) concentration in rats, and this effect was annulled by (alpha-helical)-CRH9-41, an antagonist of corticotropin-releasing hormone (CRH). The systemic administration of [D-Trp11]-neurotensin (NT-A), a specific NT antagonist, dose-dependently reduced the basal level of circulating ACTH, and this effect was blunted by NT injection. The ACTH inhibitory action of NT-A was completely overcome by the administration of CRH. Taken together, our findings suggest that NT plays a physiologic role in rats, as ACTH secretagogue, and that the mechanism underlying this action of NT involves the stimulation of CRH release.
journal_name
Life Scijournal_title
Life sciencesauthors
Nussdorfer GG,Malendowicz LK,Meneghelli V,Mazzocchi Gdoi
10.1016/0024-3205(92)90250-ssubject
Has Abstractpub_date
1992-01-01 00:00:00pages
639-43issue
9eissn
0024-3205issn
1879-0631pii
0024-3205(92)90250-Sjournal_volume
50pub_type
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