Regulation of the Vasoactive Intestinal Peptide Receptor

Rosselin, G; Anteunis, A; Astesano, A.; Boissard, Claudine; P, Gali; Hejblum, Gilles; Marie, Jean‐Claude

doi:10.1111/j.1749-6632.1988.tb26983.x

Cited by 17 publications

(3 citation statements)

References 59 publications

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“…Desensitisation to PACAP has also been demon¬ strated in rat pituitary cells in which the stimulation of growth hormone secretion by PACAP was reduced if the cells were preincubated with PACAP (Wei et al 1993). The mechanisms responsible for desensitisation to PACAP have not been investigated but, at least for VIP, desensi¬ tisation involves rapid receptor internalisation (Muller et al 1985, Boissard et al 1986, Luis et al 1986, Rosselin et al 1988). With subsequent removal of ligand, receptor number returns to almost normal within one hour (Luis et al 1986).…”

Section: Discussionmentioning

confidence: 99%

Effects of pituitary adenylate cyclase-activating polypeptide and vasoactive intestinal polypeptide on cyclic AMP accumulation in sheep pituitary cells in vitro

Sawangjaroen

Sernia²,

Curlewis³

1996

Journal of Endocrinology

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Pituitary adenylate cyclase-activating polypeptide (PACAP) and vasoactive intestinal polypeptide (VIP) are known to stimulate adenylate cyclase activity in rat pituitary cells but no direct effects have been reported on sheep pituitary cells. In this study we determined whether either peptide could stimulate intracellular cAMP accumulation in dispersed sheep pituitary cells in primary culture. Time course studies with PACAP showed that tachyphylaxis developed rapidly and so a short incubation time (5 min) was used to define the dose-response relationship. PACAP dose-dependently stimulated intracellular cAMP levels with a half-maximum response at 2.9 +/- 0.2 nmol/l (n = 4). In contrast, VIP only caused a small increase in intracellular cAMP levels at the highest dose tested (1 mumol/l). The VIP antagonist [4Cl-D-Phe6,Leu17]VIP had no effect on the cAMP response to either PACAP or VIP while the peptide PACAP(6-38), a putative PACAP antagonist, blocked the cAMP response to PACAP. The desensitisation to PACAP was further investigated by pretreating cells with PACAP for 30 min. After a further 15 min in culture medium alone, these cells showed no cAMP response to subsequent treatment with PACAP but could respond to forskolin. When a longer incubation period of 240 min was used between the first and second treatment with PACAP, a partial return in responsiveness to PACAP was observed. In summary, these results show that PACAP activates adenylate cyclase in sheep pituitary cells but that there is rapid development of tachyphylaxis. Experiments with the antagonists suggest that the response to PACAP is via the PACAP type I receptor. In contrast, physiological doses of VIP do not stimulate cAMP accumulation in sheep pituitary cells.

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Section: Discussionmentioning

confidence: 99%

Effects of pituitary adenylate cyclase-activating polypeptide and vasoactive intestinal polypeptide on cyclic AMP accumulation in sheep pituitary cells in vitro

Sawangjaroen

Sernia²,

Curlewis³

1996

Journal of Endocrinology

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“…This large molecular weight form is probably caused by post-translational processing most probably due to glycosylation as previously reported for PACAP receptors by Sone et al (1994). VlP-bindmg sites have been demonstrated on mem¬ branes from RINm5F and RIN14B insulinoma cells (Andersson et al 1992), and in rat islets (Rosselin et al 1988). The same study (Andersson et al 1992), however, reported no change in insuhn secretion from RINm5F cells in response to VIP.…”

Section: Discussionmentioning

confidence: 99%

A 67 kDa protein mediates pituitary adenylate cyclase-activating polypeptide and vasoactive intestinal peptide-stimulated insulin secretion in a hamster clonal β-cell line

Kulkarni

Smith²,

Ghatei³

et al. 1995

Journal of Endocrinology

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Insulin secretion is regulated by neural and neurohormonal factors. The report of nerves releasing pituitary adenylate cyclase-activating polypeptide (PACAP)--a 38 amino acid peptide--in the endocrine pancreas, suggests it may be important in modulating insulin release. We therefore carried out receptor-binding studies on membranes prepared from the glucose-responsive clonal beta-cell line HIT-T15, and also examined the effects of PACAP38, PACAP27--a C-terminal truncated form of the peptide--and vasoactive intestinal peptide (VIP) on insulin and islet amyloid polypeptide (IAPP) release. We showed by chemical cross-linking that PACAP and VIP stimulate secretion from the clonal cells by binding to a receptor with a molecular weight of 67 kDa (n = 4). Binding was saturable when membranes were incubated with 125I-PACAP27 (Kd 1.2 +/- 0.2 nM; Bmax 415.7 +/- 35.3 fmol/mg; n = 4) or 125I-VIP (Kd 1.3 +/- 0.3 nM; Bmax 354.8 +/- 42.8 fmol/mg; n = 4). We also demonstrated an increase in glucose-stimulated insulin (PACAP27, 366.6 +/- 25.8%; PACAP38, 389.9 +/- 13.4%; VIP, 342.6 +/- 16.1% of control; all at 1 microM, P < 0.01 vs control) and IAPP release (PACAP27, 236.9 +/- 26.2%; PACAP38, 226.5 +/- 10.9%; VIP, 242.9 +/- 15.8% of control; all at 1 microM, P < 0.01 vs control). Incubation of the cells with these peptides, for a duration of 12 h, in the presence of 5.5 mM glucose, did not alter the expression of insulin or IAPP. These findings suggest that PACAP and VIP stimulate secretion of insulin and IAPP by binding to a 67 kDa protein on clonal beta-cells and do not alter the transcription of insulin and IAPP under the conditions tested.

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“…Since suckling also stimulates the secrction of oxytocin (33) and VIP (341, these factors may also contribute to the regulation of central VIP receptors. Several rcports have suggestcd that VIP receptors are regulated by its own ligand (35)(36)(37)(38). Sustained exposure of the pineal gland to VIP in vitro decreases the number of receptors and reduces CAMP stimulation in response to VIP treatment (37).…”

Section: Discussionmentioning

confidence: 99%

Changes in Vasoactive Intestinal Peptide Binding Site Densities in the Female Rat Central Nervous System and Pituitary During Lactation

Viau

Montagne

Sarrieau

et al. 1992

J Neuroendocrinology

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Using quantitative autoradiography, vasoactive intestinal peptide (VIP) binding site densities were investigated in the female rat during lactation. Plasma prolactin levels were significantly (P<0.01) elevated on days 3 and 10 of lactation. In the brain, there was a significant (P<0.05) increase in VIP binding sites during lactation in the striatum, thalamus, anterior portion of the paraventricular nucleus of the hypothalamus, and several cortical areas compared to virgin female diestrous rats. VIP binding density in the anterior pituitary was significantly higher (P<0.01) when measured on day 3 of lactation, and decreased to diestrous levels by day 10. Pup removal resulted in a significant reversal of the lactation-induced increase in VIP binding density in the thalamus, parietal and insular cortices, and the anterior portion of the paraventricular nucleus. Taken together, modifications in VIP binding site density in the pituitary and in several central areas are associated with changes in the level of prolactin secretion. Moreover, the pattern of VIP receptor induction during lactation suggests a role for VIP in the brain that extends beyond the regulation of prolactin secretion.

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Regulation of the Vasoactive Intestinal Peptide Receptor

Cited by 17 publications

References 59 publications

Effects of pituitary adenylate cyclase-activating polypeptide and vasoactive intestinal polypeptide on cyclic AMP accumulation in sheep pituitary cells in vitro

Effects of pituitary adenylate cyclase-activating polypeptide and vasoactive intestinal polypeptide on cyclic AMP accumulation in sheep pituitary cells in vitro

A 67 kDa protein mediates pituitary adenylate cyclase-activating polypeptide and vasoactive intestinal peptide-stimulated insulin secretion in a hamster clonal β-cell line

Changes in Vasoactive Intestinal Peptide Binding Site Densities in the Female Rat Central Nervous System and Pituitary During Lactation

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