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S Arancibia

Publications and source records attributed to S Arancibia.

At least 55 records · Page 3Linked to original sources
PubMed1988

Decrease of hypothalamic TRH levels but not plasmatic TSH levels after ablation of submandibular salivary glands in the rat.

Indirect relationships are thought to exist between submandibular salivary glands (SSG) and the central nervous system (CNS) via superior cervical ganglia (SCG). To study this topic, the concentrations of thyrotropin releasing hormone (THR) and somatostatin (SRIF) were measured in both whole and specific areas of the hypothalamus, as well as plasmatic thyrotropin stimulating hormone (TSH) levels following ablation of SSG. Twenty, forty and fifty days after ablation of SSG, groups of operated and sham-operated animals weighing 230-260 g at the beginning of experimentation, were killed by cervical dislocation. Plasma was taken, frozen and stored for TSH-radioimmunoassay (RIA) and the hypothalami were removed and homogenized in either 0.1 N HCl (for TRH-RIA) or 0.2 N acetic acid (for SRIF-RIA). Twenty days after ablation of SSG in another group, TRH concentrations were measured in both the median eminence (ME) and the paraventricular nucleus (PVN), dissected by the micropunch technique. The results show that twenty days after SSG ablation, the hypothalamic TRH concentrations was significantly lower in operated than in sham-operated animals (295.2 +/- 24.8 vs 226 +/- 11.15 pg/mg hypothalamus respectively p less than 0.01, n = 9). No differences were observed at later intervals. This finding seems to be specific for this peptide since the SRIF level was not modified twenty days after SSG removal. Among the discrete hypothalamic areas examined, only the ME exhibited a significant decrease in TRH content (25.43 +/- 3.02 ng/mg prot. VS. 41.24 +/- 1.33 ng/mg prot., respectively). Despite these results on TRH levels, no modifications in plasmatic TSH levels were observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Somatostatin-immunoreactive concentrations in human saliva and in the submandibular salivary glands of the rat. Possible sexual dependence in the human.

Many biologically active polypeptides have been detected either in the submandibular salivary glands (SSG) of the rat, and in the saliva of rats and humans. The present work has investigated the case of somatostatin (SRIF), since salivary data concerning the presence of this peptide are scarce and contradictory. In a group of healthy volunteers, SRIF-immunoreactivity (SRIF-IR) was tested in samples of mixed saliva. Not all the subjects revealed presence of SRIF-IR in saliva. For men, 5 out of 9 were positive (x = 26.40 +/- 10.03 pg/ml), whereas for women only one out of 10 was positive (x = 96.40 pg/ml). SRIF-IR was also determined in male rat submandibular glands from control animals (26.1 +/- 6.3 pg/mg protein, n = 18) and from animals injected one hour before with an alpha 1-adrenergic secretagogue, phenylephrine (27.9 +/- 7.1 pg/mg protein, n = 6). The results show that SRIF-IR is not constantly present in human saliva obtained from a young population, and that its presence apparently seems to differ between the sexes. On the other hand, the fact that SRIF-IR, unlike other peptides, is not modified when the animals are injected with phenylephrine, may simply indicate that the control mechanism of SRIF-IR release is not the same as that affecting other salivary peptides. Further studies must be carried out in order to elucidate the origin and role of salivary SRIF-IR.

Adolescent↗
PubMed1987

["Push-pull" perfusion technic in neuroendocrinology].

In this article the author reviews the different models of push-pull cannula device used in neuroendocrinology, mainly those applied to the study of neurohormones release from median eminence (ME). At present, three technical details might explain some disagreements resulting from application of push-pull perfusion (PPP) in neuroendocrinology, concerning for instance, the SRIF release: firstly, the tissue damage connected with the diameter of the cannulas utilized (guide and perfusion), secondly, the perfusion flow which can vary from 15 to 40 microliter/min according to the authors, and finally, the means of implanting the cannula in the ME (between 8 days and 1 hour before perfusion). The author compares the values of SRIF, TRH and CRF releases measured by portal cannula with those obtained by PPP. It would seem that the application of a physiological stimulus triggers a response measured in the perfusate whose amplitude as compared to basal levels, is more important than the amplitude measured in portal blood. In conclusion, in despite of its limits--reproductiveness and yield--, at the present time PPP may be considered one of the major methodological tools affording the physiologist optimum conditions for in vivo studies.

Animals↗
PubMed1987

[Secretion of TRH in the third cerebral ventricle during acute cold exposure in the unanesthetized rat. Effect of alpha-adrenergic drugs].

The concentrations of TRH in the cerebrospinal fluid (CSF) of the 3rd ventricle were measured with push-pull cannulae in 12 conscious rats. In the basal state the level of TRH in 15 min perfusion samples (210 microliters) were low (2.69 +/- 0.05 pg) and mostly undetectable with the RIA available. However, 70 to 80 min after exposure of the rats to cold (4 degrees C) a short lived but significant rise of TRH was measured in all animals. Post cold peaks amounted to 5.15 +/- 0.5 pg/15 min (p less than 0.001 vs baseline levels). This cold response to CSF TRH was influenced neither by pretreatment of rats with the alpha-adrenergic blocker phentolamine, administered i.p. (40 mg/kg) or i. c. v. (10(-5) M) 1 h before cold exposure, nor by i. c. v. infusion of the alpha 1-adrenergic blocker prazosin (10(-5) M). In rats receiving the blockers the post-cold TRH peaks were 6.76 +/- 1.61 pg/15 min and 5.70 +/- 0.70 pg/15 min, respectively. The possible origin of CSF TRH and the resistance of its cold stimulation to alpha-adrenergic blockers, compared to TRH released into the median eminence are discussed.

Animals↗
PubMed1987

[Evaluation of an in vivo perfusion technic for the dental pulp in rats as validated by demonstration of the release of prostaglandins].

Many different biologically active substances contribute to the metabolism of dental pulp. Until now, release of these substances has been evaluated only by in vitro studies. The aim of this study was to establish a technique of perfusion allowing the evaluation in vivo of the secreting activity of dental pulp. In order to validate this technique, the in vivo release of prostaglandins, substances which seem to play a key role in pulpal metabolism was measured. The "push-pull" perfusion technique was used, whereby a physiological medium was made to bath the pulpal surface by aspiration. Pulp was exposed by opening an upper incisor in an anaesthetized rat. The perfusion was kept constant by means of a device composed of cannula, catheters, and micropumps which produced a flow followed by an aspiration of the liquid. Every ten minute fraction was analysed by high performance liquid chromatography. Ten minutes after the beginning of perfusion, the results showed a kinetic for PGE2 and PGF2 alpha release, characterized by a base level of 7.4 +/- 6.7 and 28.6 +/- 12.0 pg/min respectively. These were interrupted by a very high peak as compared to base level (19 times higher for PGE2 and 6.6 times for PGF2 alpha), occurring fifty minutes after trepanation. This experiment is the first attempt made in vivo and in situ, to measure biologically active substances of pulpal origin.

Animals↗
PubMed1986

Effects of morphine on cold-induced TRH release from the median eminence of unanesthetized rats.

The effect of morphine perfusion into the median eminence on cold-induced TRH secretion was studied in unanesthetized rats by push-pull cannulation. Perfusion with 10(-6)M morphine blocked the cold-induced TRH peak occurring about 40 min after the transfer of rats from 24 degrees C to 4 degrees C. This inhibition by morphine was blunted by concomitant administration of naloxone (10(-6)M or 10(-5)M), but naloxone alone had no effect on either basal or cold-induced TRH release. We conclude that specific opiate receptors may be located on TRH nerve endings in the ME, and that endogenous opiates may not have any physiological role in the cold-induced TRH response, at least during the two hours that follow cold exposure.

Animals↗
PubMed1986

Probable extrapituitary source of the immunoreactive prolactin measured in the cerebrospinal fluid of unanesthetized rats by push-pull cannulation of the 3rd ventricle.

The dynamic pattern of the immunoreactive prolactin (PRL) concentrations in the cerebrospinal fluid (CSF) of the 3rd ventricle was explored by push-pull cannulation during either stimulation or blocking of PRL production in the plasma, which itself was sampled by chronic cannulation of the carotid. Some of the results were compared to the PRL concentrations in CSF samples obtained by 3rd-ventricle puncture. Ether stress, which induced a 4- to 6-fold rise in plasma PRL, altered neither the pulsatile circhoral pattern of PRL in the CSF nor the mean level and amplitude of its pulses. However, the sustained intense hyperprolactinemia induced by haloperidol increased the mean PRL level in the CSF and possibly its pulse rate. Surprisingly, hypophysectomy, which suppressed production of PRL in the plasma, did not alter its baseline level or cycling pattern in the CSF. The possibility that tuberal adenohypophysial cells and/or CNS prolactinergic neurons supply the CSF with PRL is discussed.

Animals↗
PubMed1986

Effect of submandibular salivary gland removal on body weight, plasmatic testosterone levels, testicular weight and spermatogenesis in rats.

In this work we report the effect of the removal of submandibular salivary glands (S.S.G.) on plasmatic testosterone levels and other aspects of testicular function and on body weight in rats. Our results were obtained with 72 male rats weighing 230-260 g whose S.S.G. were removed. At only twenty days after removal a slight but significant decrease (p less than 0.05) of testicular absolute weight (3.431 +/- 75 mg vs 3.612 +/- 53 mg) was detected. This decrease was probably due to atrophy of interstitial tissue, as revealed by histological examination. In contrast, neither plasmatic testosterone (T) levels nor spermatogenesis (S.P.G.) were altered. The effect on testicular weight at twenty days was not closely associated with the effect on body weight. Changes in this latter parameter were observed twenty days after extirpation of S.M.G. (107 +/- 5.5 vs 124 +/- 4.3 g; p less than 0.02) and up until forty days (175.6 +/- 4.1 g vs 202.8 +/- 5.5; p less than 0.05) after S.S.G. removal. Difference in gain of body weight is not influenced by nutritional lack, as shown by the fact that nutritional absorption is not modified in the operated animals controlled in wire bottom cages. These data suggest that S.S.G. right play a trophic regulatory role, separately, on testes and body without the mediation of T. The direct involvement of biological peptides contained in S.S.G. is discussed.

Animals↗
PubMed1985

Evidence for alpha 1-adrenergic stimulatory control of in vitro release of immunoreactive thyrotropin-releasing hormone from rat median eminence: in vivo corroboration.

The aim of this study was to investigate whether the alpha-adrenergic stimulation of TSH secretion may occur directly at the median eminence (ME) level by modulating the release of TRH. The effects of pharmacological manipulations of the two subtypes of central alpha-adrenergic receptors, alpha 1 and alpha 2, were tested on in vitro TRH release from medial basal hypothalami containing mainly the ME. Hypothalamic fragments were superfused with a modified Locke medium, and TRH was measured by RIA in samples collected every 10 min. After a preliminary period of 40 min to test TRH release during basal conditions, drug effects were checked for 20 min. Superfusion with norepinephrine (NE) (10(-10), 10(-8), 10(-6) M) induced a rapid and dose-dependent rise of TRH release; epinephrine (10(-8) M) induced an effect similar to that of NE 10(-8) M. Phentolamine (10(-7) M), an alpha-adrenergic antagonist, completely blocked the NE (10(-8) M)-induced release of TRH, which was not modified by the beta-adrenergic antagonist propranolol (10(-7) M). Neither antagonist had an effect on basal TRH release when added alone to the medium. The NE-induced release of TRH was completely suppressed by prazosin (10(-7) M), whereas yohimbine had no effect. Superfusion with clonidine (10(-9), 10(-8), 10(-7), 10(-6) M), an alpha 2-receptor agonist, did not alter basal TRH release. In contrast, phenylephrine (10(-8) and 10(-6) M), an alpha 1-receptor agonist, induced a significant (P less than 0.01) rise in TRH release. These results were corroborated in vivo in several unanesthetized rats bearing a push-pull cannula previously and stereotaxically implanted into the ME. Perfusion with artificial cerebrospinal fluid containing NE (10(-7), 10(-6) M) or phenylephrine (10(-7) M) elicited a rapid rise in TRH release, within 15 min after the onset of drug perfusion. Clonidine (10(-5) M), similarly perfused for 15 min, had no effect. Our data suggest a direct stimulatory influence of catecholamines on TRH release at the ME level that is mediated through alpha 1-adrenergic receptors.

Animals↗
PubMed1985

[Submaxillary glands in an endocrine context].

The evidence for interrelationships between the submandibular salivary glands (SMG) and the endocrine system is reviewed. Firstly, it has been clearly demonstrated that various hormones participate in the molecular control of exocrine enzyme synthesis in the SMG, and more particularly within the cells of the convoluted granular tubules of the gland. Testosterone was thus shown to stimulate the synthesis of a series of SMG enzymes via its specific cellular receptors and the genetic machinery of protein synthesis, while the active thyroid hormone T3, together with the glucocorticosteroids act synergistically with testosterone. In addition, experimental evidence is accumulating, ascribing to the SMG an endocrine function. More specifically, two important hormonal factors appear to originate in the SMG: the nerve growth factor (NGF), a polypeptide of 140.000 d which is highly concentrated in the SMG and plays a major role in the ontogenetic development and in the functions of spinal and sympathetic ganglia; and the epidermal growth factor (EGF), a 6.045 d peptide displaying a variety of biological actions including promotion of epidermal development, eruption of the incisors, stimulation of pituitary secretion of ACTH and GH, and inhibition of gastric and of thyroid hormone secretion. As previously observed for the SMG exocrine enzymes production, the two endocrine secretions of the SMG are also controlled by various classical hormones such as testosterone, thyroid hormones and adrenocorticosteroids. Finally, a more complex regulatory loop involving the SMG hormones was recently described, including a retrograde axonal transport of NGF from the SMG to the superior cervical ganglion (SCG) where it participates in transmitter syntheses, and, beyond the SCG, in the control of various targets of the SCG such as the pineal gland and other neuroendocrine regulations. Summing up, the buccal segment presently appears as a mixed glandular section with both exocrine and endocrine functions in the same line as the lower segments of the digestive tract, i.e. stomach, duodenum, liver and pancreas.

Adrenal Cortex Hormones↗
PubMed1985

[Demonstration of prolactin flow into the cerebrospinal fluid of the alert rat in a pulsatile circhoral manner by push-pull cannulation of the 3d ventricle].

In 8 male unanesthetized rats, sequential sampling of cerebrospinal fluid (CSF) from a push-pull cannula implanted into the 3rd ventricle revealed that prolactin was present in this fluid, where it displayed circhoral pulsatility resembling the temporal variations in plasma prolactin observed in the same animals. Although basal prolactin levels were lower in the CSF than in the plasma, the amplitude of the circhoral prolactin pulses was twice as great in the CSF as in the plasma compartment. The possible origin and role of CSF prolactin are discussed.

Animals↗
PubMed1984

In vivo release of somatostatin from rat median eminence after local K+ infusion or delivery of nociceptive stress.

The effects of local infusion of a 16 mM K+ solution or of a nociceptive stress on the release of somatostatin (SRIF) from the hypothalamus was measured in unanesthetized male rats implanted with a push-pull cannula in the median eminence. Although the baseline secretion rate of SRIF was increased in animals displaying agitation as a result of handling stress, both treatments induced fast doubling of SRIF release lasting for 15-30 min. Neither an equimolar Na+ infusion into the median eminence nor a similar K+ infusion into the 3rd ventricle had any affect on this release. The possible role of SRIF release in the mechanism of growth hormone inhibition following nociceptive stress is discussed.

Animals↗
PubMed1984

K+-induced thyrotropin-releasing hormone release from superfused mediobasal hypothalami in rats. Inhibition by somatostatin.

Somatostatin (SRIF), in concentration of 10(-6) M, significantly inhibited the depolarization-induced release of immunoreactive thyrotropin-releasing hormone (IR-TRH) from superfused mediobasal hypothalami (MBH) containing mainly the median eminence (ME), without affecting the basal release of TRH. The total amount of K+-induced TRH release was 0.24 +/- 0.02 and 0.61 +/- 0.08 pg/MBH/min, respectively, in the presence and absence of SRIF in the medium. The data are consistent with a role of SRIF as a neuromodulator on TRH release from the ME. In contrast, superfusion with Locke medium containing triiodothyronine (10(-6) M) had no effect on basal and K+-induced IR-TRH release in our system.

Animals↗
PubMed1983

[Demonstration of pulsatile secretion of somatostatin in the third cerebral ventricle of unanesthetized rats].

Using a specially designed push-pull cannula stereotaxically implanted into the 3rd ventricle, a pulsatile secretion of IR-SRIF with a circhoral periodicity was detected in male rats. At 30 min. to 1 h 1/2 intervals the secretion rate of the neuropeptide rose from a baseline rate of 14.5 +/- 0.5 pg/10 min., corresponding to a baseline concentration of 60 +/- 2 pg/ml to peaks of 50 +/- 5 pg/10 min. or 210 +/- 22 pg/ml, respectively. This pulsatile pattern was restricted to rats where histological examination showed no dilation pictures of the ventricle. The possible origin and function of intra-ventricular IR-SRIF are discussed.

Animals↗
PubMed1983

Direct evidence of short-term cold-induced TRH release in the median eminence of unanesthetized rats.

IR-TRH release in the median eminence was directly estimated in conscious rats during the first 130 min of exposure to cold (4 degrees C), using a push-pull cannulation. A three-fold increase in IR-TRH release was observed, with a peak of 10.00 +/- 2.19 pg/15 min occurring 40 min after exposure to cold; control rats, left at 24 degrees C, stayed at the baseline secretion rate of 3.40 pg/15 min which was the sensitivity limit of the RIA assay.

Animals↗
PubMed1982

Neurotensin stimulation of prolactin secretion in vitro.

Neurotensin stimulated prolactin (PRL) secretion from incubated rat hemipituitaries. Under the same conditions, the secretion of growth hormone, luteinizing hormone and follicle-stimulating hormone was not affected. The stimulation of PRL was dose dependent, with an apparent affinity of neurotensin of 0.56 +/- 0.12 nM and a maximal stimulation of 56.5 +/- 6.7%. The effect of neurotensin seemed to be independent of that of other PRL releasing factors. In fact, the stimulation of neurotensin and thyrotropin-releasing hormone (TRH) and also of neurotensin and vasoactive intestinal peptide were additive. The action of neurotensin on PRL cells does not appear to involve either dopamine or gamma-aminobutyric acid receptors, since antagonists to these transmitters were found ineffective on PRL stimulation by neurotensin. PRL-releasing factor activity distinct from TRH has been described in fractions of hypothalamic extracts. Neurotensin, which is present in high amounts in the median eminence and has been measured in the adenohypophysis, is a candidate as a physiological PRL-releasing factor distinct from TRH.

Animals↗