Vasoactive intestinal peptide (VIP) stimulates prolactin (PRL) release and cAMP production in a rat pituitary cell line (GH3/B6). Additive effects of VIP and TRH on PRL release

Gourdji, D.; Bataille, D.; Vauclin, N.; Grouselle, Dominique; Rosselin, G; Tixier‐Vidal, A.

doi:10.1016/0014-5793(79)81107-2

Cited by 166 publications

(55 citation statements)

References 26 publications

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“…In [7,8] VIP receptors in the pituitary were coupled to cAMP, and the increase of cAMP accumulation was related to stimulation of PRL secretion [7,8]. However, conflicting data have been reported regarding the involvement of cAMP in the mechanism of action of SRIF [13].…”

Section: Discussionmentioning

confidence: 99%

“…On the other hand, vasoactive intestinal peptide (VIP) has been reported to stimulate specifically PRL release from rat pituitary lactotrophs [6]. It appears that this effect is mediated by cyclic AMP (cAMP) [7,8]. Here, we investigated whether SRIF can interact with the stimulatory effect of VIP on PRL release by rat pituitary cells in culture, and whether this action is mediated by a modification of the cAMP accumulation induced by VIP.…”

Section: Introductionmentioning

confidence: 99%

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Rapid inhibition by somatostatin of vasoactive intestinal peptide‐induced prolactin secretion by rat pituitary cells

Rostène¹,

Dussaillant²,

Rosselin³

1982

FEBS Letters

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Rapid inhibition by somatostatin of vasoactive intestinal peptide‐induced prolactin secretion by rat pituitary cells

Rostène¹,

Dussaillant²,

Rosselin³

1982

FEBS Letters

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“…Receptors for VIP have been identified in many tissues including the pituitary , and in all sites at which VIP is active the receptor is coupled with adenyl cyclase so that there is activation of cyclic AMP (Gourdji et al, 1979;Bjoro et al, 1987). Growth hormone releasing hormone, which has structural similarities with VIP, especially in the rat, recognizes VIP receptors in some tissues but not in the normal pituitary cells (Robberecht et al, 1986).…”

Section: The Cellular Actions O F Vipmentioning

confidence: 99%

“…The best-known stimulator of prolactin release is TRH. When VIP is added in combination with TRH either in uitro (Gourdji et al, 1979) or in uiuo (Prysor-Jones er al., 1984) the stimulatory effect is either synergistic with TRH or additive according to the type of rat pituitary tumour that is studied.…”

Section: Vip and The Action O F Other Factors I N The Regulation Of Pmentioning

confidence: 99%

Vasoactive Intestinal Peptide and Anterior Pituitary Function

Prysor-Jones

Jenkins

1988

Clinical Endocrinology

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Vasoactive intestinal peptide (VIP) is a highly basic 28 amino‐acid peptide which was first isolated from porcine small intestine (Said & Mutt, 1970). It is related to several other peptides including PHI (peptide with N‐terminal histidine and C‐terminal isoleucine amide), secretin, glucagon, and has some sequences similar to those of growth hormone releasing hormone (Fig. 1). The amino‐acid sequence of human VIP is identical with that of the porcine form (Itoh et al., 1983). It has been shown that human VIP is cosynthesized with PHM (peptide with N‐terminal histidine and C‐terminal methionine amide, the human analogue of PHI) from the same large precursor protein (Itoh et al., 1983).

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“…DA was also shown to affect calcium and potassium fluxes in those cells (18). These phenomena are likely to be implicated in the mechanism o f action of DA on PRL release since, in addition to cyclic AMP (CAMP) production (19)(20)(21)(22) and modulation of phosphatidylinositol phosphate breakdown (23)(24)(25)(26), regulation of PRL secretion is dependent on calcium entry into lactotrophs (27,28).…”

mentioning

confidence: 99%

Interaction of Opiate Peptides with Dopamine Effects on Prolactin Secretion and Membrane Electrical Properties in Anterior Pituitary Cells from Lactating Rats

Enjalbert

Israël

Zhang

et al. 1990

J Neuroendocrinology

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Met-enkephalin and b-endorphin induced a partial reversion of the dopamine inhibition of prolactin release from pituitary cells of lactating rats in primary culture. This effect of opiate peptides was dose-dependent with an EC50 of 40f8 nM and 4 5 + 7 nM and maximal blockade of dopamine inhibition of 60% and 68% for Met-enkephalin and /]-endorphin, respectively. Naloxone antagonized the effect of Met-enkephalin with an EC50 of 22_$12 nM. Furthermore, this Met-enkephalin effect on dopamine inhibition of prolactin secretion appeared non-competitive since it reduced maximal inhibition without affecting the apparent affinity of dopamine. Finally, it should be noted that the two opiate peptides had no effect on spontaneous prolactin release.In electrophysiological experiments, local ejection of dopamine on tested cells induced an hyperpolarization concomitant with an increase of the membrane conductance. Ejection of Met-enkephalin or /&endorphin alone did not modify the electrical properties of the cells (resting potential, membrane conductance and excitability). In contrast, both peptides blocked in a reversible manner the dopamine-induced electrical responses. These effects were antagonized by naloxone. However, this interaction of opiate peptides with dopamine electrical response was not observed on all cells tested. We conclude that the blocking effect of opiates on dopamine-induced hyperpolarization may account, at least in part, for the ability of these peptides to interact with dopamine inhibition of prolactin release.Prolactin (PRL) release is under a tonic inhibitory control by dopamine (DA) (1). Opiates have been shown to interact with DA inhibition of PRL secretion both at the hypothalamic (2-4) and pituitary level (5 -8). I n the anterior pituitary, morphine and opiate peptides had no effect on the spontaneous PRL release (9, 10) but reversed inhibition of secretion induced by DA. Although this was not observed under all experimental conditions (1 l), this effect seems to involve a specific opiate receptor since it has been shown to be blocked by opiate antagonists ( 5 , 6, 8). In addition, spccific opiate binding sites have been described in anterior pituitary membranes (12, 13), although they could not be fully characterized because of the important contamination of endogenous B-endorphin-like peptides (14).Recently, it has been shown that DA induced a hyperpolarizing response due to a n increased potassium conductance on human (1 S), bovine (16) and rat lactotrophs ( I 7). During this response spontaneous calcium action potentials were suppressed (17). DA was also shown to affect calcium and potassium fluxes in those cells (18). These phenomena are likely to be implicated in the mechanism o f action of DA on PRL release since, in addition to cyclic AMP (CAMP) production (19-22) and modulation of phosphatidylinositol phosphate breakdown (23-26), regulation of PRL secretion is dependent on calcium entry into lactotrophs (27,28).An effect of morphinomimetic peptides on the DA hyperpolarization of ...

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Vasoactive intestinal peptide (VIP) stimulates prolactin (PRL) release and cAMP production in a rat pituitary cell line (GH3/B6). Additive effects of VIP and TRH on PRL release

Cited by 166 publications

References 26 publications

Rapid inhibition by somatostatin of vasoactive intestinal peptide‐induced prolactin secretion by rat pituitary cells

Rapid inhibition by somatostatin of vasoactive intestinal peptide‐induced prolactin secretion by rat pituitary cells

Vasoactive Intestinal Peptide and Anterior Pituitary Function

Interaction of Opiate Peptides with Dopamine Effects on Prolactin Secretion and Membrane Electrical Properties in Anterior Pituitary Cells from Lactating Rats

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