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S Arancibia

Publications and source records attributed to S Arancibia.

47 records · Page 3Linked to original sources

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

[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

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

[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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