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Biomedical subjects

C Rivier

Publications and source records attributed to C Rivier.

At least 199 records · Page 11Linked to original sources
PubMed1983

In vitro and in vivo ACTH-releasing activity of ovine CRF, sauvagine and urotensin I.

The ability of three homologous peptides, ovine corticotropin-releasing factor (CRF), sauvagine and urotensin I, to release ACTH was examined in vitro and in vivo. All three peptides exhibit statistically equivalent potencies to stimulate ACTH secretion both by cultured pituitary cells and in pharmacology blocked rats. These results suggest that all three peptides evolved from a common mammalian precursor that possessed high hypophysiotropic potency.

Adrenocorticotropic Hormone↗
PubMed1983

Comparison of the effect of several gonadotropin releasing hormone antagonists on luteinizing hormone secretion, receptor binding and ovulation.

The biological activity of three gonadotropin releasing hormone (GnRH) antagonists was evaluated in the following assays: suppression of GnRH-mediated luteinizing hormone (LH) secretion by cultured pituitary cells, suppression of the spontaneous LH release by ovariectomized rats, blockade of ovulation in regularly cycling females and inhibition of binding of a potent radiolabeled agonist to rat pituitary membrane homogenates. The peptides were: [Ac-delta 3Pro1,4FDPhe2, DTrp3,6]-GnRH (Antagonist 1); [Ac-delta 3Pro1,4FDPhe2,DNAL(2)3,6]-GnRH (Antagonist 2); and [Ac-DNAL(2)2,4FDPhe2,DTrp3,DArg6]-GnRH (Antagonist 3). All three antagonists exhibited similarly high potency in suppressing LH secretion in vitro, while Antagonist 1 was the most active peptide in the radioreceptor assay. When administered by gavage, Antagonist 3 exhibited the highest potency to inhibit LH secretion in gonadectomized rats and to block ovulation. Comparison of the oral versus the subcutaneous mode of administration of these analogs indicates that less than 1% is absorbed after gavage. However, these data demonstrate that the intragastric administration of GnRH antagonists can lower gonadotropin secretion and interfere with reproductive functions.

Administration, Oral↗
PubMed1983

Influence of ethanol on reproductive functions of the adult male rat as a function of body weight.

Adult male rats were exposed to alcohol vapors for 3-4 weeks. Blood alcohol levels (BAL) ranged from 90 to 190 mg/100 ml. BAL of greater than or equal to 0-130 mg/100 ml were compatible with adequate body weight gains and were not associated with diminished plasma testosterone (T) levels or reduced sex organ weights. BAL greater than or equal to 180 mg/100 ml were associated with inhibition of androgen secretion only in those animals who failed to grow. From these results we conclude that in growing animals, the medium term exposure to ETOH leads to inhibition of reproductive parameters when high BALs induce weight loss, but not when adequate body growth is maintained.

Animals↗
PubMed1983

Isolation, analysis of structure, synthesis, and biological actions of urotensin I neuropeptides.

The 41-residue neuropeptide urotensin I (UI), from the urophyses of two teleost fish species (Cyprinus carpio and Catostomus commersoni), was isolated and purified, and its amino acid sequence was determined and confirmed by synthesis of a fully active peptide. The UI peptide was found to be a close structural and biological homologue of the ovine hypothalamic corticotropin-releasing factor (CRF) and the frog skin peptide sauvagine; UI is, therefore, a phylogenetic prototype of this group of peptides. Extraction of urophyses in hot acetic or hydrochloric acid cleaves an amino terminal tripeptide yielding a fully active UI(4-41). The UI peptides are equipotent with the other two naturally occurring peptides (CRF and sauvagine) in the release of mammalian pituitary corticotropin (ACTH), but UI is several times more potent than the mammalian homologue in the stimulation of release of fish pituitary ACTH. The UI peptide and its mammalian or amphibian homologues have a long-lasting hypotensive action in mammals, via a uniquely selective vasodilatation in the superior (anterior) mesenteric vascular bed only. The significantly lower hypotensive vasodilatory action of the mammalian homologue (CRF) suggests a change in the unknown physiological role of the haemodynamic actions of the UI peptides in the mammalian gastrointestinal tract during phylogenetic progression from fishes to mammals.

Adrenocorticotropic Hormone↗
PubMed1983

Effect of synthetic ovine corticotropin-releasing factor. Dose response of plasma adrenocorticotropin and cortisol.

Synthetic ovine corticotropin-releasing factor (CRF) was administered to normal male volunteer subjects as an intravenous bolus or 30-s infusion. Doses of CRF ranging from 0.001 to 30 micrograms/kg body wt were administered, and plasma immunoreactive (IR)-ACTH and IR-cortisol concentrations were measured. The threshold dose appeared to be 0.01-0.03 micrograms/kg, the half-maximal dose 0.3-1 micrograms/kg, and the maximally effective dose 3-10 micrograms/kg. Basal concentrations of IR-ACTH and IR-cortisol were 14 +/- 7.6 pg/ml (mean +/- SD) and 5.6 +/- 2.2 micrograms/dl, respectively. IR-ACTH rose as early as 2 min after CRF injection, reached peak levels in 10-15 min, and declined slowly thereafter. IR-cortisol rose at 10 min or later and reached peak levels in 30-60 min. At a dose of 30 micrograms/kg, neither IR-ACTH nor IR-cortisol fell from peak levels of 82 +/- 21 pg/ml (mean +/- SE) and 23 +/- 1.4 micrograms/dl, respectively, during the 2-h course of the experiment, indicating that CRF has a sustained effect on ACTH release and/or a prolonged circulating plasma half-life. There was little or no increase in the levels of other anterior pituitary hormones. At doses of 1 microgram/kg and higher, facial flushing, tachycardia, and, in some subjects, a 15-29-mmHg decline in systemic arterial blood pressure were observed, even though blood volume was replaced and the subjects remained supine. These data indicate that synthetic ovine CRF is a very potent and specific ACTH secretagogue in man. Administered with caution until its vasomotor effects are more fully defined, CRF promises to be a safe and very useful investigative, diagnostic, and, possibly, therapeutic agent in man.

Adrenocorticotropic Hormone↗
PubMed1983

Effects of synthetic ovine corticotropin-releasing factor, glucocorticoids, catecholamines, neurohypophysial peptides, and other substances on cultured corticotropic cells.

Synthetic ovine corticotropin-releasing factor (CRF) is a 41-residue peptide with high potency and intrinsic activity to stimulate the secretion of ACTH and beta-endorphin-like immunoactivity (beta-End-LI) by cultured adenohypophysial corticotropic cells. The action of CRF in vitro can be potentiated by the weaker secretagogues, vasopressin, oxytocin, epinephrine, norepinephrine, and angiotensin II. CRF-mediated secretion of ACTH and beta-End-LI is noncompetitively inhibited by pretreatment of cells with glucocorticoids. Long term exposure of adenohypophysial cells to CRF results in an increase in total medium plus cell ACTH in the cultures, suggesting that CRF can enhance rates of ACTH synthesis as well as release. CRF also stimulates the secretion of beta-End-LI by corticotropic cells cultured from the neurointermediate lobe. Higher concentrations of CRF are required to stimulate secretion by this cell type than by anterior lobe corticotropic cells. These in vitro results are consistent with CRF playing a major physiological role in the neuroregulation of secretion by anterior lobe corticotropic cells, where the peptide may interact with other modulators.

Adrenocorticotropic Hormone↗
PubMed1983

Interaction of corticotropin-releasing factor and arginine vasopressin on adrenocorticotropin secretion in vivo.

A possible interaction between synthetic ovine corticotropin-releasing factor (CRF) and arginine vasopressin (AVP) was tested in anesthetized and in freely moving rats. In animals whose endogenous CRF release was blocked by chlorpromazine-morphine-nembutal, AVP elicited a significantly lower maximum ACTH response than did CRF, whereas the concomitant injection of both peptides resulted in a marked potentiation of CRF-induced ACTH secretion. In freely moving rats, AVP was more potent than CRF (on an equimolar basis) in elevating plasma ACTH levels. Since immunoneutralization of endogenous CRF by the administration of anti-CRF serum significantly reduced ACTH release due to injected AVP in these animals, we suggest that at least part of the AVP-induced ACTH secretion observed in nonanesthetized rats may be due to a potentiation of endogenous CRF by exogenously administered AVP. These data support previous reports of an in vitro synergism between CRF and vasopressin, and emphasize the complex role played by the interaction of these two peptides on ACTH release in vivo.

Adrenocorticotropic Hormone↗
PubMed1983

Influence of the frequency of ovine corticotropin-releasing factor administration on adrenocorticotropin and corticosterone secretion in the rat.

We have examined the pattern of ACTH secretion in rats receiving two or more injections of synthetic ovine corticotropin-releasing factor (CRF). A first exposure of cannulated intact rats to CRF caused a blunting of the ACTH response when CRF was again injected 0.5-6 h later. Since plasma corticosterone levels stayed elevated for only 2 h after the first injection of CRF, the diminished pituitary responsiveness persisted at a time when plasma corticosterone levels had returned to control values. When cannulated adrenalectomized animals were subjected to a similar treatment, the blunting of the ACTH release due to the second injection of CRF, though present, was of significantly shorter duration. Duplication of the corticosterone levels that follow one CRF injection by exogenous administration of the steroid inhibited the subsequent ACTH response to CRF for a maximum of 2 h. Finally, CRF infused into intact rats for 14 days consistently caused elevation of both ACTH and corticosterone secretion. We conclude that CRF administered in a repeated or continuous manner to intact rats, while causing some pituitary desensitization, still elicits a significant degree of ACTH secretion despite the presence of elevated corticosterone release. This observation as well as the fact that CRF-injected adrenalectomized animals exhibit some blunting of their ACTH responses suggest that steroid feedback, while participating in the diminished ability of CRF to repeatedly stimulate ACTH release, does not represent the sole modulator of pituitary responsiveness.

Adrenalectomy↗
PubMed1982

Inhibition of adrenocorticotropic hormone secretion in the rat by immunoneutralization of corticotropin-releasing factor.

Intravenous administration of rabbit antiserum to ovine corticotropin-releasing factor (CRF) markedly reduced the CRF-induced rise of plasma adrenocorticotropic hormone (ACTH) in intact nonstressed adult male rats while blocking more than 75 percent of the ACTH release observed in rats exposed to ether stress. Furthermore, antiserum to CRF significantly lowered ACTH levels in adrenalectomized animals. These results suggest that endogenous CRF plays a physiological role in regulating ACTH secretion.

Adrenalectomy↗
PubMed1982

In vivo and in vitro effects of tetrahydroisoquinolines and other alkaloids on rat pituitary function.

Several tetrahydroisoquinolines (TIQs) were tested for their in vitro and in vivo capacities to modulate prolactin (PRl) and beta-endorphin (beta-end) secretion by the rat pituitary and for their abilities to displace [3H]spiroperidol and [3H]naloxone binding from pituitary and hypothalamic membranes. Receptor binding studies showed that TIQs could be classified as having (a) higher affinity for opiate receptors (tetrahydropapaverine, papaverine, 6-methylsalolinol, 1-carboxysalsolinol and 3',4'-deoxy-norlaudanosolinecarboxylic acid), (b) higher affinity for the dopamine receptor (salsolinol and 7-methylsalsolinol), or (c) approximately equal affinity for the two binding sites (6,7-dimethylsalsolinol and tetrahydropapaveroline, THP). In freely moving male rats, THP produced a several-fold increase in plasma PRL levels. This effect was not altered by co-administration of naloxone but was attenuated by dopamine. In vitro several TIQs reversed the inhibitory effect of dopamine on PRL secretion by cultured anterior pituitary cells. The order of potencies of the TIQs in this system paralleled their order of potencies in the dopamine receptor assay. THP, the most potent dopamine antagonist, also blocked dopamine-mediated inhibition of beta-endorphin secretion from neurointermediate lobe cells in culture. These data demonstrate that THP and some other TIQs can act as dopamine antagonists in radioreceptor assays, in cell culture and in vivo.

Animals↗
PubMed1982

Corticotropin-releasing factor: effects on the sympathetic nervous system and oxygen consumption.

Corticotropin-releasing factor administered intracerebroventricularly produces prolonged elevation of plasma concentration of epinephrine, norepinephrine and glucose. These hormonal changes are associated with an increase in motor activity and oxygen consumption. No change in body temperature is observed. CRF produces changes in animal physiology that are similar to those observed in response to stress.

Animals↗
PubMed1982

Comparison of the biologic actions of corticotropin-releasing factor and sauvagine.

Corticotropin-releasing factor (CRF), a peptide isolated from ovine hypothalamus, and sauvagine, a peptide isolated from frog skin, share significant structural homology and elicit a number of similar biological responses. CRF is more potent than sauvagine in stimulating pituitary ACTH secretion. Sauvagine, however, is 5-10 times more potent than CRF to act within the brain to increase plasma levels of catecholamines and glucose and to elevate mean arterial pressure. Sauvagine is likewise more potent than CRF to act outside the brain to increase superior mesenteric artery flow and plasma glucose concentrations and to decrease mean arterial pressure. CRF and sauvagine produce important effects representative of biologically active peptides.

Adrenocorticotropic Hormone↗
PubMed1982

In vivo corticotropin-releasing factor-induced secretion of adrenocorticotropin, beta-endorphin, and corticosterone.

A 41-residue peptide purified as a corticotropin-releasing factor/beta-endorphin-releasing factor (CRF) in vitro was tested for its ability to stimulate the secretion of ACTH, beta-endorphin, and corticosterone in three animal groups: 1) unanesthesized rats bearing indwelling venous cannulae, 2) rats pretreated with chloropromazine plus morphine sulfate plus pentobarbital (CPZ-MS-Nb, and 3) rats with hypothalamic deafferentiations in the frontal and lateral retrochiasmatic areas. In all three bioassays iv administration of 0.1-10 micrograms CRF elicited a dose-related increase in plasma ACTH and beta-endorphin values over a 5- to 15-min period. Corticosterone secretion was also elevated but responded maximally with all doses of CRF tested. Pretreatment of CPZ-MS-Nb animals with 20 micrograms dexamethasone 4 h before assay abolished the CRF-induced hormone secretion. These data suggest that CRF may play a physiological role in the regulation of the hypothalamic-pituitary-adrenal axis.

Adrenocorticotropic Hormone↗
PubMed1982

Interaction of gonadotropin-releasing hormone agonist and antagonist with progesterone, prolactin, or human chorionic gonadotropin during pregnancy in the rat.

Two GnRH analogs, one agonist and one antagonist, have been administered to pregnant female rats with or without concomitant treatments with progesterone (Po), PRL, or hCG. During the first week of gestation, Po was consistently capable of totally reversing the deleterious effect of the agonist, while PRL and hCG were slightly less effective. During the second week of pregnancy, only Po and hCG were effective. When the antagonist was injected during either the first or second week after mating, both Po and hCG could prevent the abortifacient action of the analog, while PRL was without effect. These data suggest that the antigestational properties of gonadotropin-releasing hormone agonists are at least partially mediated through inhibition of PRL secretion, while those of gonadotropin-releasing hormone antagonists do not appear to be. Additionally, hCG as well as Po proved capable of counteracting the antigonadal effects of both classes of analogs.

Animals↗