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B Briaud

Publications and source records attributed to B Briaud.

At least 19 recordsLinked to original sources
PubMed1981

[Vasopressin and "CRF" in the regulation of ACTH secretion by the anterior and intermediate lobes of the pituitary gland (author's transl)].

The aim of this review was to summarize the present state of knowledge concerning the mode of action of vasopressin (VP) and the putative corticotropin releasing factor (CRF) on ACTH secretion from the anterior and intermediate lobes of the pituitary gland. In vitro data show that although both CRF and VP enhanced release of anterior pituitary ACTH, the pattern of hormonal release, based on kinetical and dose-dependent studies, appeared to be different. Also, the effect of VP most probably was mediated by specific putative receptor sites. In contrast, VP was found not to alter ACTH secretion from the intermediate lobe; that secretion seems to be regulated by CRF-like material and neurotransmitters. The importance of VP as a corticotropin agent is discussed.

Adrenocorticotropic Hormone↗
PubMed1981

Glucocorticoid binding and control ACTH secretion.

This report attempts to summarize the present state of knowledge concerning interaction of glucocorticoids with brain and pituitary receptors, in relation to induction of specific biological effects. It examines the properties of the receptors, emphasizing the fact that transcortin-like binding molecules are present on the cell membrane in the pituitary gland. Also, it considers the functional aspects of the mechanism of action of steroids, including control, occupancy and heterogeneity of binding sites, as well as correlation with regulation of ACTH release.

Adrenocorticotropic Hormone↗
PubMed1980

Involvement of vasopressin in corticotropin-releasing effect of hypothalamic median eminence extract.

Incubation of anterior pituitary (AP) fragments of rats was used to determine the specific role played by vasopressin (VP) in the overall effect of crude hypothalamic median eminence (HME) extract on ACTH release. Using the property of an AVP antiserum (AS) to completely abolish the CRF-like effect of hypothalamic VP without apparently affecting the effect of CRF, we show that under specific incubation conditions, the effect of the two secretagogues are additive at the pituitary level. ACTH secretion of pituitaries was enhanced when incubation was carried out in the presence of VP together with a maximum effective dose of VP-free HME extract (from Brattleboro rats). These observations favor the hypothesis that VP and CRF have different receptor sites in the anterior pituitary.

Adrenocorticotropic Hormone↗
PubMed1980

In vitro regulation of ACTH release from neurointermediate lobe of rat hypophysis. III. Effect of potassium (K+), calcium (Ca++) and dibutyryl cyclic 3',5'-adenosine monophosphate (dbc-AMP).

Alterations in the ionic composition of the medium and different secretagogues have been used in order to study the mechanism of release of ACTH from superfused neurointermediate lobes (NIL) of rat hypophysis. We showed that: (a) a tenfold increase of K+ in the medium caused a reversible and repeatable stimulation of the ACTH release; (b) removal of Ca++ reversibly abolished the stimulating effect of high K+; (c) removal of Ca++ had no effect on the stimulating effect of a hypothalamic extract (HE); (d) in the latter case, a reversible significant weakening was obtained by the addition of EDTA in the Ca++-free medium; (e) dbc-AMP caused a reversible and repeatable stimulation of the ACTH release; (f) comparable results were obtained for anterior lobes (AL) superfused in the same conditions. From these data we can conclude that Ca++ is necessary for the stimulation of the hormonal release and that factors such as K+ or dbc-AMP can mimic the in vitro stimulating effect of a HE. Similarities, which appear in this study, between the modulation of the ACTH release from NIL and AL, led us to support the idea that, in vivo, a release of ACTH from the NIL, may occur in physiological conditions.

Adrenocorticotropic Hormone↗
PubMed1980

Effect of steroids on vasoactive intestinal peptide in discrete brain regions and peripheral tissues.

The effect of castration and adrenalectomy was studied on vasoactive intestinal peptide (VIP) concentrations in various brain and peripheral structures of male rats. Castration has no effect on any of the structures studied, whereas 4 weeks adrenalectomy (ADX) decreases VIP concentrations in the hippocampus and increases them in the adenohypophysis, two structures known to contain large amounts of glucocorticoid receptors. Corticosterone administration restores VIP levels to control values only in the dorsal hippocampus. In contrast, dexamethasone counteracts both the decrease and the increase of VIP concentrations obtained after ADX in the hippocampus and in the adenohypophysis respectively. The present results suggest that corticosteroids can be involved in the regulation of VIP actions both in the brain and in the adenohypophysis.

Adrenalectomy↗
PubMed1980

[Specificity of the effect of vasopressin at the anterior pituitary level (author's transl)].

The present investigation was conducted in order to get more insight into the mechanism of action of vasopressin (VP) on ACTH secretion and characterize VP interaction with putative receptor sites at the level of the anterior pituitary gland. The experimental procedure consisted of increasing ACTH release from incubated pituitary fragments as induced by VP in the presence or absence of oxytocin (OT) and various releasing factors. Our results show that, whereas OT was able to depress VP-induced release of ACTH (Fig. 2), TRF (Fig. 3), LH-RH (Fig. 4) and crude "CRF" extract (Fig. 1) it did not exhibit any significant inhibitory effect. This provides indirect evidence for the presence of specific pituitary sites for VP and related peptides such as OT. The latter, however, was devoided of corticotrophic releasing properties.

Adrenocorticotropic Hormone↗
PubMed1979

Effects of adrenalectomy and hypercorticism on the ACTH content of the anterior and posterior pituitary in rats with inherited diabetes insipidus (Brattleboro strain).

The effects of adrenalectomy (Adx) and hypercorticism on the ACTH content in the anterior (AH) and the neurointermediate lobe (NIL) of the pituitary in Long Evans (+/+), heterozygous (+/DI) and homozygous (DI/DI) Brattleboro rats were determined using dispersed adrenal cells bioassay. Adx decreased the NIL-ACTH content in +/DI and DI/DI rats and left it unchanged in the +/+ rats. Adx increased the AH-ACTH content in the three groups. Hypercorticism had a delayed decreasing effect both in the AH and in the NIL in all rats, with one exception for the NIL in DI/DI rats. Conversely to what appeared in Wistar rats, in Long Evans and Brattleboro rats the corticosterone administered in drinking water was unable to reduce the increase in AH-ACTH activity. These data suggest that Brattleboro, and, to a lesser extent, Long Evans rats from which the former are derived present some particularities in the regulation of their corticotropic function at the AH and the NIL level. We also observed that NaCl (0.9%) added to drinking water and hypercorticism are two factors able to increase diabetes insipidus in homozygous rats without modifying the water intake in Long Evans and heterozygous rats.

Adrenal Glands↗
PubMed1979

Relationship between ACTH secretion and corticoid binding to specific receptors in perifused adenohypophyses.

This study reports on the kinetics of glucocorticoid-induced inhibition of ACTH release, together with steroid binding to specific pituitary receptors. It was shown that corticosterone (CORT) inhibited ACTH output provoked by either corticotropin-releasing factor (CRF) extracts or dbcAMP, in a manner which was both dose- and time-dependent. A close correlation appeared to exist between the degree of ACTH blockade and the percentage of filled steroid-binding sites. However, exposure of hypophyses to CORT for a critical period of time was a prerequisite for such a relationship to develop. Furthermore, it was found that dexamethasone (DEX) was more potent than CORT in inhibiting ACTH secretion and, in addition, bound to a greater extent to nuclei of pituitary cells. These data suggest the existence of a close correlation between occupancy of pituitary glucocorticoid receptors and modulation of ACTH secretion.

Adrenocorticotropic Hormone↗
PubMed1979

Different effects of K+ and Ca++ on alpha-MSH and ACTH release from superfused neurointermediate lobe of the rat hypophysis.

The effects of K+-enhanced and Ca++-free media on alpha-MSH and adrenocorticotropic hormone (ACTH) release from superfused neurointermediate lobe (NIL) were studied in the same experiments. High K+ caused reversible and repeatable inhibition of alpha-MSH release and stimulation of ACTH release, Removal of Ca++ impaired the effect of K+, irreversibly for alpha-MSH and reversibly for ACTH. The existence of both melanotrophic and corticotrophic cells within the intermediate lobe (IL) of rat hypophysis could account for the different effects of ionic modifications on in vitro alpha-MSH and ACTH release.

Adrenocorticotropic Hormone↗
PubMed1979

Subcellular distribution of corticotropin-releasing factor in the medio-basal hypothalamus of the rat.

Subcellular fractionation of the mediobasal hypothalamus (MBH) and frontal cerebral cortex was performed by differential and discontinuous sucrose gradient centrifugation. Corticotropin-releasing factor (CRF) activity of the different fractions was evaluated by bioassay. Significant CRF activity was found in acidic extracts of the MBH but not of the cerebral cortex. About 80% of the MBH effect on adrenocorticotropic hormone release was recovered in the crude mitochondrial pellet (P2) which contains synaptosomes. After further fractionation, distribution of CRF activity paralleled that of lactate dehydrogenase activity, a marker of the soluble cytoplasm. It is concluded that most CRF in the MBH is located in nerve endings as already shown for several other neurohormones.

Animals↗
PubMed1979

In vitro regulation of ACTH release from neurointermediate lobe of rat hypophysis. II. Effect of neurotransmitters.

The effect of various neurotransmitters on adrenocorticitropic hormone (ACTH) release from superfused neurointermediate lobes of rat hypophysis (NIL) was investigated. Acetylcholine, serotonin, and histamine were shown to have no significant effect on the spontaneous release of ACTH. In contrast, dopamine (DA) and noradrenaline (NA) stimulated NIL ACTH release in a dose-dependent manner. The stimulating effect of DA was mimicked by apomorphine and inhibited by haloperidol, whereas that of NA was abolished by phentolamine. In a comparative study, none of these neurotransmitters is shown to have any significant stimulating effect on ACTH release from superfused anterior lobes. It is concluded that the ACTH release from NIL might be controlled, at least in part, by catecholaminergic innervation.

Acetylcholine↗
PubMed1978

In vitro regulation of ACTH release from neurointermediate lobe of rat hypophysis. I. Effect of crude hypothalamic extracts.

Using incubated glands, we showed that cerebral cortex and liver extracts (CCE and LE) stimulated ACTH release from neurointermediate lobe (NIL) of hypophysis as well as hypothalmus extract (HE) did. Moreover, the HE-induced ACTH release was much smaller for the NIL (1.9 X basal level) than for the anterior lobe (AL; 13.7 x basal level). Thus, under these conditions, HE seemed to have no specific effect on NIL ACTH release. Using superfused glands, we showed: (a) that both spontaneous and HE-induced ACTH release decreased during superfusion; (b) that using this system, a specific stimulatory effect on HE on NIL was observed. In contrast to HE, CCE and LE had only a small effect on NIL ACTH release (always less than 20% of that caused by HE) which could be considered as a nonspecific response; (c) that trypsin suppressed the stimulating effect on HE as well on NIL as on AL; and (d) that arginine antidiuretic hormone (ADH) was not responsible for the stimulating effect of HE on NIL ACTH release, because synthetic ADH had no effect and HE containing ADH (from normal rats) or HE containing no ADH (from Brattleboro rats or from immunoneutralization of ADH in normal HE) had the same effect. From these results, we can conclude that HE contain a peptidic factor different from ADH which is able to stimulate in vitro release of ACTH from the NIL.

Adrenocorticotropic Hormone↗
PubMed1978

Inverse effects of corticosterone and thyroxine on glucocorticoid binding sites in the anterior pituitary gland.

The aim of this study was to determine whether pituitary glucocorticoid binding sites are under hormonal control. It was shown that corticosterone and thyroxine exerted antagonistic effects on both the transcortin-like component and true receptor present in the hypophysis: thyroid hormones, in contrast to glucocorticoids which exhibited opposite influence, increased maximum binding without affecting significantly the apparent association constant. Thus, it seems that the concentration of glucocorticoid binding sites is regulated by the glucocorticoid ligands, as well as by a different hormone. Moreover, a striking parallelism was found between plasma transcortin and pituitary transcotin-like capacity, argueing in favour of a plasma origin for this pituitary binder.

Adrenalectomy↗
PubMed1978

Specific interaction of corticosteroids with binding sites in the plasma membranes of the rat anterior pituitary gland.

The binding of glucocorticoids to a crude fraction of rat pituitary plasma membranes and to solubilized membrane proteins was measured. The binding characteristics were similar to those exhibited by transcortin: radioactive corticosterone was bound to a greater extent than radioactive dexamethasone and labelled corticosterone, but not labelled dexamethasone, was displaced by unlabelled corticosterone, deoxycorticosterone and progesterone. A Scatchard plot of the binding data revealed the presence of a binding material with a dissociation constant of about 3.2 nmol/l, which sedimented at 4S after sucrose density-gradient centrifugation. It was found that the number of binding sites was inversely related to the concentration of corticosterone in the circulation and was increased after long-term adrenalectomy. These data suggest that a material similar to transcortin is complexed to the plasma membrane of rat pituitary cells.

Adrenalectomy↗
PubMed1976

Heterogeneity of pituitary glucocorticoid binding evidence for a transcortin-like compound.

Scatchard analysis, as well as sucrose gradient centrifugation demonstrate that at least two classes of specific glucocorticoid binding sites occur in the adenohypophysis. One, exhibited high affinity for both corticosterone and dexamethasone (receptor D), while the other bound only corticosterone. The latter binder revealed physico-chemical properties closely similar to those of plasma transcortin, but was shown not to be due to simple blood contamination of cytosol. This transcortin-like (TL) component, however, seemed to be carried over from plasma, since the concentration of pituitary binding sites strikingly paralleled physiological variations of plasma transcortin. Furthermore, experiments carried out with isolated pituitary cells suggested an intracellular location of that binder, although sticking to the cell membrane cannot be excluded. Finally, it was shown that the TL compound was unable, unlike the receptor D, to transfer glucocorticoids into the nuclei. One of its possible roles could be to modulate the interaction between steroids and compound D.

Adrenal Glands↗