Autoparacrine action of vasoactive intestinal peptide on dopaminergic control of prolactin secretion.
We have previously reported that pituitary vasoactive intestinal peptide (VIP) mediates through autoparacrine mechanisms insulin-like growth factor-I and TRH-stimulated PRL release. In the present study, we have investigated whether VIP might also be implicated in the PRL increase that follows dopamine (DA) withdrawal. The experiments were carried out in defined medium supplemented or not with T3, as in a previous study we had found that PRL release increases under low T3 culture conditions due to mediation by concomittant stimulus of VIP. Anterior pituitary (AP) cells from adult male rats were incubated for 1 h in the presence of DA (10 microM), a VIP-receptor antagonist (VIP-At) (200 nM), or DA plus VIP-At. Then media were removed and the cells were washed with PBS and reincubated under the same conditions but without the addition of DA. In the first incubation, DA inhibited PRL release by 80%, and VIP release by 20% in both T3-free and T3 medium. In the second period of incubation, PRL and VIP release were increased in AP cells previously exposed to DA. These effects were greater when the cells were cultured in T3-free medium than in T3-medium (225% and 150%, respectively for PRL release; and 155 and 135%, respectively for VIP release). PRL response to DA withdrawal was inhibited by the simultaneous presence of VIP-At. This inhibition was again greater when the cells were incubated in medium supplemented with T2. Thus, the stimulus of DA withdrawal was inhibited by 88% in T2-free medium and by 37% in T3-medium. To investigate whether pituitary VIP messenger RNA (mRNA) expression is under dopaminergic control, AP cells were incubated in the presence or absence of bromocriptine (BC) (10 nM) for 2 and 24 h. After 24 h of incubation, BC decreased mRNA levels of PRL and of the two transcripts which VIP expresses in AP. As with DA, BC also inhibited PRL and VIP release both at 2 and 24 h. These data demonstrate that VIP, at least partially, mediates DA withdrawal-induced PRL release through an autoparacrine action. They also suggest that simultaneous inhibition of pituitary VIP mRNA expression and VIP release may be a necessary mechanism for the dopaminergic inhibition of PRL mRNA expression and PRL release.
Balsa
J A
JA
Servicios de Endocrinología, Centro Nacional Investigaciones Clinicas, Instituto Carlos III, Madrid, Spain.
Sánchez-Franco
F
F
Lorenzo
M J
MJ
Pazos
F
F
Lara
J I
JI
Cacicedo
L
L
D000818:Animals; D001971:Bromocriptine / Q000494:pharmacology; D002478:Cells, Cultured; D004298:Dopamine / Q000008:administration & dosage / Q000494:pharmacology / Q000502:physiology*; D015870:Gene Expression / Q000187:drug effects; D006801:Humans; D008297:Male; D010903:Pituitary Gland, Anterior / Q000166:cytology / Q000187:drug effects / Q000378:metabolism; D011388:Prolactin / Q000235:genetics / Q000378:metabolism*; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D018005:Receptors, Vasoactive Intestinal Peptide / Q000037:antagonists & inhibitors; D014284:Triiodothyronine / Q000494:pharmacology; D014660:Vasoactive Intestinal Peptide / Q000235:genetics / Q000378:metabolism / Q000502:physiology*
D012333:RNA, Messenger; D018005:Receptors, Vasoactive Intestinal Peptide; D014284:Triiodothyronine; D014660:Vasoactive Intestinal Peptide; D001971:Bromocriptine; D011388:Prolactin; D004298:Dopamine