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S Arancibia

Publications and source records attributed to S Arancibia.

69 records · Page 4Linked to original sources
PubMed1982

Reciprocal interactions of somatostatin with thyrotropin-releasing hormone and vasoactive intestinal peptide on prolactin and growth hormone secretion in vitro.

Reciprocal interactions of somatostatin (SRIF) and vasoactive intestinal peptide (VIP) or TRH on in vitro PRL and GH release from male rats hemipituitaries were investigated. SRIF did not modify basal PRL release, but TRH- or VIP-induced release was inhibited by SRIF in a dose-dependent manner [effective concentration-fifty (EC50) = 1.7 +/- 0.9 nM for SRIF inhibition of TRH stimulation and EC50 = 0.8 +/- 0.5 nM for SRIF inhibition of VIP stimulation]. VIP and TRH did not affect GH release by themselves, but reduced the inhibition of GH secretion elicited by SRIF (EC50 = 7.6 +/- 3.4 nM for TRH blockade of SRIF inhibition and EC50 = 4.6 +/- 3.1 nM for VIP blockade of SRIF inhibition). Secretin, a partial structural analog of VIP, also blocked SRIF-induced inhibition of GH and stimulated PRL release. Secretin stimulation of PRL release was also prevented by SRIF. [D-Trp8,D-Cys14]SRIF, a potent analog of SRIF, antagonized VIP stimulation of PRL secretion with the same apparent affinity as the native peptide. The maximal stimulation, but not the apparent affinity of VIP action on prolactin release was reduced by SRIF, suggesting that the interaction is of a noncompetitive nature. This conclusion as further substantiated by the observation that neither TRH nor VIP were able to displace specific 125I-labeled [Tyr1] SRIF high affinity binding to pituitary membranes. The three peptides tested thus appear to exhibit reciprocal interactions mediated by independent receptor sites on GH as well as on PRL-producing cells.

Animals↗
PubMed1981

[PRF activity of VIP in vitro (author's transl)].

The effect of VIP on prolactin secretion from incubated rat hemipituitaries was characterized. Under these conditions, the secretion of GH, LH, FSH, ACTH was not affected, indicating that the effect of VIP is hormone specific. The stimulation of prolactin was dose-dependent, with an apparent affinity of VIP of 10.9 +/- 3.1 nM and a maximal stimulation of 57.7 +/- 4.2%. Secretin, a structurally related peptide, was also active at higher concentrations, whereas another partial analogue, glucagon, was ineffective. Furthermore, VIP does not act through pituitary DA receptors since alpha-flupentixol, a potent dopaminergic antagonist, does not block the stimulation of prolactin secretion by VIP. In addition, stimulation by VIP and TRH was additive. Naloxone and met-enkephalin were ineffective on the VIP effect on prolactin release. In contrast, SRIF seems to inhibit the VIP stimulation of prolactin release. Our data suggest that VIP, which was found in the hypothalamo-hypophyseal blood at concentrations of the same order of magnitude as that found to stimulate PRL in vitro, could be a physiological PRF.

Animals↗
PubMed1980

Stimulation of in vitro prolactin release by vasoactive intestinal peptide.

VIP stimulated prolactin secretion from incubated rat hemipituitaries. Under the same conditions, the secretion of GH, LH, FSH was not affected. The stimulation of prolactin was dose-dependent, with an apparent affinity of VIP of 10.9 +/- 3.1 nM and a maximal stimulation of 57.7 +/- 4.2%. Secretin, a structurally related peptide, was also active at higher concentrations whereas another partial analogue, glucagon, was ineffective. The effect of VIP was not blocked by alpha-flupentixol, a potent dopaminergic antagonist, at concentrations which antagonized the dopamine inhibition of prolactin secretion. Stimulation by VIP and TRH was additive. Neither Met-enkephalin nor naloxone interfered with the response to VIP. It thus seems that specific VIP receptors are present on pituitary prolactin cells. VIP, present in the mediobasal hypothalamus and detected in the hypothalamo-hypophyseal portal blood therefore is a good candidate as a physiological PRF.

Animals↗
PubMed1980

[Effect of neuropeptides on prolactin secretion by the adenohypophysis (author's transl)].

In order to identify prolactin regulating factors, the effect of various neuropeptides on prolactin secretion by the adenohypophysis has been tested. 1 degree Histidyl-proline-diketopiperazine (DKP), a major degradation product of TRH in hypothalamus and pituitary, inhibited prolactin secretion from incubated hemipituitaries (Fig. 1) with an apparent affinity of 0.5 nM. Histidyl-prolineamide and histidyl-proline, other degradation products of TRH, had no effect. TSH secretion was not affected under the same conditions. 2 degrees Vasoactive intestinal peptide (VIP) stimulated prolactin secretion in vitro in a dose dependent manner. The secretion of other adenohypophyseal hormones was not affected. This effect is not mediated by a dopaminergic mechanism, since it was not blocked by neuroleptics (Table I). 3 degrees Morphinomimetic peptides had no effect on prolactin secretion in vitro, but blocked the dopamine inhibition of prolactin secretion. The effect of metenkephalin and beta-endorphin was dose dependent and was blocked by naloxone (Fig. 2 and 3). Thse results indicate that specific receptors to various neuropeptides seem to be present on prolactin cells.

Animals↗
PubMed1979

Independent inhibition of prolactin secretion by dopamine and gamma-aminobutyric acid in vitro.

gamma-Aminobutyric acid (GABA) inhibits PRL release from incubated hemipituitaries in a dose-dependent manner. The maximum inhibition obtained with GABA is less than that obtained with dopamine. Its affinity is 100 times lower. The effect is blocked by picrotoxin but not by a dopamine inhibitor; alpha-flupentixol but not picrotoxin antagonizes dopamine inhibition. This indicates that dopamine and GABA inhibit PRL release through independent receptors. The hypothalamic extract contains sufficient GABA to inhibit PRL release in our in vitro conditions. Picrotoxin, however, does not significantly inhibit the nondopaminergic PRL-inhibiting activity of mediobasal hypothalamic extracts. Another nondopaminergic PRL-inhibiting factor, therefore, seems to be present in the hypothalamus.

Animals↗
PubMedDate not supplied

[Salivary hormones: a new aspect of oral physiology].

Aside from the digestive enzymes the submandibular salivary glands (SSG) synthetize other polypeptides, detected also in saliva, with varied biological activity; NGF and EGF are the knowest. However, over the last decade, steroids hormones have been also found out in the saliva at the same concentrations that the free plasma fraction. The origin of these hormones is largely discussed and certain authors have even proposed a local synthesis for them. This matter, is of clinical interest because gingiva and buccal tissues are knowingly sensitive to steroids. Besides, woman ovulation appears to be monitored through progesterone fluctuations in saliva. Another kind of salivary substances is formed by the neuropeptides of the gut-brain axis, mainly VIP and SRIF. The former likely of nervous origin seems to be involved in the atropine-resistant salivary secretion, whereas the latter-likely of SSG origin--appears as a factor associated with glycemia control.

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