AUTOCRINE AND OR PARACRINE ACTION OF VASOACTIVE-INTESTINAL-PEPTIDE ONTHYROTROPIN-RELEASING HORMONE-INDUCED PROLACTIN-RELEASE/

Citation
Ja. Balsa et al., AUTOCRINE AND OR PARACRINE ACTION OF VASOACTIVE-INTESTINAL-PEPTIDE ONTHYROTROPIN-RELEASING HORMONE-INDUCED PROLACTIN-RELEASE/, Endocrinology, 137(1), 1996, pp. 144-150
Citations number
47
Categorie Soggetti
Endocrynology & Metabolism
Journal title
ISSN journal
00137227
Volume
137
Issue
1
Year of publication
1996
Pages
144 - 150
Database
ISI
SICI code
0013-7227(1996)137:1<144:AAOPAO>2.0.ZU;2-K
Abstract
Several in vitro studies have demonstrated that vasoactive intestinal peptide (VIP) modulates basal PRL release in normal and hypothyroid an terior pituitary (AP) cells through an autocrine or paracrine action. As thyroid hormone is an important factor in the regulation of pituita ry VIP synthesis and secretion, we analyzed the influence of the absen ce of thyroid hormone on basal PRL release in vitro to study whether t he release of PRL induced by TRH might be mediated by a local action o f pituitary VIP. When normal AP cells were cultured in a medium supple mented with a near-physiological concentration of free T-3 (0.5 nM), b asal PRL and VIP release decreased and PRL secretion was not altered b y the blockade of VIP action. This finding allowed us to establish the culture conditions in which basal PRL secretion is apparently not und er VIP influence. Consequently, we were able to study whether pituitar y VIP may be implicated in TRH-induced PRL release. TRH(100 nM) increa sed PRL and VIP release in a parallel manner and decreased PRL and VIP intracellular content in incubations from 15-180 min. When AP cells w ere incubated simultaneously with TRH and a VIP receptor antagonist, T RH-induced PRL release decreased when incubation lasted more than 30 m in, whereas the depletion of PRL intracellular content induced by TRH was unchanged. TRH also slightly increased VIP messenger RNA levels at 3 and 24 h, but PRL messenger RNA levels were not modified. These dat a demonstrate that pituitary VIP participates in TRH-induced PRL relea se and that the effect of thyroid hormone on basal pituitary VIP secre tion should be borne in mind when studies on its effect, through autoc rine and/or paracrine mechanisms, on PRL release stimulated by PRL-rel easing factors are conducted.