Immunoreactive Vasoactive Intestinal Polypeptide in Rat Hypophysial Portal Blood

Shimatsu, Akira; Kato, Yuzuru; Matsushita, Norio; Katakami, Hideki; Yanaihara, Noboru; Imura, Hiroo

doi:10.1210/endo-108-2-395

Cited by 126 publications

(31 citation statements)

References 16 publications

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“…The overall average of these values equalled 58 ± 7 nM for VIP with the monkey pituitary cells. This half-maximal effective concentra tion of VIP is similar to that reported for rat hemipituitaries [ ~ 10 nM, from 2] and monkey hemipituitaries [ ~ 25 nM, from 3), but less than the ED50 reported for human adenomas [300 nM, from 4], For further comparison, the level of VIP in portal blood of rats after total hypophysectomy equalled 1,735 pg/ml under pentobarbital anesthesia [23]. This is equal to ~0.62 nM VIP which is 80 fold lower than the half-maximal dose reported here.…”

Section: Discussionsupporting

confidence: 83%

Effect of Vasoactive Intestinal Peptide on Monkey Prolactin Secretion and Cyclic AMP in Culture: Interaction with Estradiol and Phenol Red

Bethea

1990

Neuroendocrinology

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To test the hypothesis that estrogenic compounds may decrease the sensitivity of primate lactotropes to adenylate cyclase-mediated secretagogues, the effect of VIP on prolactin secretion and cAMP levels in serum-free monkey pituitary mono-layer cultures was examined in the presence and absence of estradiol (E) and phenol red. In two experimental designs, E treatment was initiated on either the day after dispersion (split plate design) or 10 days after serum-free culture (whole plate design). VIP challenges (5, 50 and 500 nM) were administered for 4 h on days 10 and 20 of culture. There was a significant decrease in the maximal percent stimulation of prolactin by VIP when cultures were treated with E or phenol red. The average percent increase in prolactin at 5, 50 and 500 nM VIP equalled 23, 83 and 156% in the absence of phenol red, but equalled 14, 43 and 112% when E was added to phenol red-free cultures. The percent stimulation by VIP in the presence of phenol red averaged 32, 62 and 97%, but addition of E with phenol red decreased the average stimulation to 26, 45 and 72%, respectively. Basal levels of cAMP were increased by E and phenol red. However, the maximal percent stimulation of cAMP by VIP was decreased in the presence of E and phenol red. In summary, E and phenol red act to decrease the maximal percent stimulation of prolactin secretion by VIP. This effect is reflected by a decrease in the maximal percent stimulation of intracellular cAMP.

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Section: Discussionsupporting

confidence: 83%

Effect of Vasoactive Intestinal Peptide on Monkey Prolactin Secretion and Cyclic AMP in Culture: Interaction with Estradiol and Phenol Red

Bethea

1990

Neuroendocrinology

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“…The physiological relevancy of the rapid modulatory action of glucocorticoids on VIP action is supported by the facts that (i) the effect of VIP on cAMP accumulation is significant at concentrations of VIP close to those found in the hypothalamopituitary blood system (36,37), and (ii) corticosterone is able to inhibit VIP-induced cAMP production in the range of steroid concentrations found in peripheral rat plasma (33). VIP recently has been shown to stimulate PRL release in man (38).…”

Section: Discussionmentioning

confidence: 99%

Rapid glucocorticoid inhibition of vasoactive intestinal peptide-induced cyclic AMP accumulation and prolactin release in rat pituitary cells in culture.

Rotsztejn¹,

Dussaillant²,

Nobou³

et al. 1981

Proc. Natl. Acad. Sci. U.S.A.

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Vasoactive intestinal peptide (VIP) stimulates both adenosine 3',5'-cyclic monophosphate (cAMP) accumulation and prolactin release in normal rat pituitary cells in culture. cAMP accumulation is significant (P < 0.01) at VIP concentrations as low as 1 nM and reaches a maximum with 0.1 ,IM. Addition of dexamethasone as early as 15 min before VIP inhibits VIP stimulation of both cAMP production and PRL secretion. The rapid inhibition is dose-dependent: it appears at doses as low as 0.01 pM and is complete at 1 pM dexamethasone. Increasing concentrations of dexamethasone induce a noncompetitive type of inhibition, as shown by the decrease in Vm.,. with no change in the apparent K.for VIP. Cycloheximide (1 mM) counteracts the inhibitory effect of dexamethasone on VIP-induced cAMP production, which suggests the involvement ofa rapid protein synthesis mechanism. Ru-26988, a specific glucocorticoid devoid of any mineralocorticoid activity and which does not bind to intracellular transcortin-like component, also produces an inhibition of VIP-induced cAMP accumulation. Corticosterone also inhibits VIP-induced cAMP production but at concentrations higher than those ofdexamethasone. In contrast, aldosterone, progesterone, estradiol, and testosterone have no effect. These results demonstrate that, in normal rat pituitary cells in culture, glucocorticoids at physiological concentrations rapidly inhibit the cAMP production and prolactin release induced by VIP by acting through specific glucocorticoid receptors.Vasoactive intestinal peptide (VIP) (9,10).In the light of both in vivo and in vitro experiments (6, 11), we suggested that corticosteroids could be involved in the regulation of VIP action on the adenohypophysis. We had previously shown that addition of dexamethasone (Dex) for 2 days to cultures of enriched pituitary rat lactotrophs completely abolished the stimulatory effect ofVIP on PRL secretion (6). Therefore, we have investigated (a) the involvement of the cAMP system in the biological effect of VIP on PRL release, (b) the kinetics and the stoichiometry of the interaction between VIP and corticosteroids, and (c) the mechanism by which Dex inhibits PRL release at the pituitary level.In the present communication, we present evidence that, in normal rat pituitary cells in culture, Dex at concentrations as low as 1 pM rapidly inhibits both the cAMP accumulation and the PRL release induced by VIP, by acting through specific glucocorticoid receptors. MATERIALS AND METHODSIsolation and Cell Culture. Male Wistar rats (45-60 days old) were used. Fifteen to 20 anterior pituitaries were minced in small pieces and dispersed enzymatically by incubation in 15-20 ml of minimal essential medium with Earle's salts containing 0.1% trypsin (1:250) (GIBCO) and 0.1% fatty acid-free bovine serum albumin (Sigma) for 2 hr at 370C (12) at pH 7.5 in a silicone-treated Bellco spinner flask. Cells were filtered though 100-,um-mesh nylon to remove DNA of broken cells and centrifuged at 400 g for 5 min; the pellet was resuspended, w...

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“…One hundred pl of plasma was used for the measurement of each sample. Plasma VIP concentrations were measured by a specific radioimmunoassay according to the method of SHIMATSU et al (1981) with a slight modification. We used synthetic porcine VIP as the standard (4110-V, Peptide Institute, Japan) and anti-VIP serum (Otsuka Pharmaceuticals, Japan) at a final dilution of 1:100,000.…”

Section: Methodsmentioning

confidence: 99%

Cholinergic and VIPergic vasodilator actions of parasympathetic nerves on the thyroid blood flow in rats.

et al. 1987

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The present experiment was performed to investigate the effect of stimulating the parasympathetic superior laryngeal nerve (SLN) on thyroid blood flow and its mediator substances in urethane-chloralose anesthetized rats. Thyroid blood flow was measured by counting number of blood drops from a thin catheter inserted into the thyroid vein. SLNs were cut bilaterally and their peripheral portions were electrically stimulated. Electrical stimulations (intensity, 10 V; pulse duration, 0.5 ms) of SLNs increased thyroid blood flow in a frequency-dependent manner as stimulus frequencies increased from 2 to 40 Hz. The intravenous administration of atropine (0.5 mg/kg) reduced these responses, but did not abolish them. The basal secretion rate of vasoactive intestinal peptide (VIP). from thyroid glands in the resting state was nearly zero (0.25 ± 0.14 pg/(kg • min)). SLN stimulation increased markedly the VIP secretion rate to 3.40 + 0.64 pg/(kg • min). The VIP secretion responses evoked by SLN stimulation remained in atropinized rats. Furthermore, exogenously applied VIP increased the thyroid blood flow dosedependently. These results suggest that SLN stimulation increases the thyroid blood flow by dilating thyroid blood vessels via activation of cholinergic and non-cholinergic (probably VIP-containing) nerve fibers. Thus, these parasympathetic vasodilation systems may play a supplementary role in regulating the secretion of thyroid hormone by changing the thyroid blood flow in addition to the role of hormonal regulation by the thyroid stimulating hormone (TSH).

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Immunoreactive Vasoactive Intestinal Polypeptide in Rat Hypophysial Portal Blood

Cited by 126 publications

References 16 publications

Effect of Vasoactive Intestinal Peptide on Monkey Prolactin Secretion and Cyclic AMP in Culture: Interaction with Estradiol and Phenol Red

Effect of Vasoactive Intestinal Peptide on Monkey Prolactin Secretion and Cyclic AMP in Culture: Interaction with Estradiol and Phenol Red

Rapid glucocorticoid inhibition of vasoactive intestinal peptide-induced cyclic AMP accumulation and prolactin release in rat pituitary cells in culture.

Cholinergic and VIPergic vasodilator actions of parasympathetic nerves on the thyroid blood flow in rats.

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