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S Arancibia

Publications and source records attributed to S Arancibia.

At least 37 records · Page 2Linked to original sources
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↗
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↗
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↗