Search PubMed⌕ Search

Biomedical subjects

F Boudouresque

Publications and source records attributed to F Boudouresque.

50 records · Page 3Linked to original sources
PubMed1982

[Opiate peptides of the adrenal medulla (author's transl)].

Significant concentrations of enkephalins are present in the adrenal medulla, notably in man, ox and dog. High molecular weight peptides precursors of enkephalin pentapeptide can also be demonstrated in the same tissue. Although the biosynthesis of enkephalins has not yet been completely elucidated, it seems to follow a pathway different from that of beta-endorphin. The secretion of enkephalins is regulated by the same mechanisms as the secretion of catecholamines. Enkephalins act locally by modulating catecholamine release, but since they are released into the systemic circulation, another, still ill-defined hormonal action is possible.

Adrenal Medulla↗
PubMed1982

Influence of endogenous somatostatin on growth hormone and thyrotropin secretion in neonatal rats.

When gestating rats were injected iv with an antiserum to somatostatin (SRIF-AS) during the last week of gestation, serum GH levels in fetuses and 6-h-old newborn rats were not significantly different from controls. Similarly, 2 h after the ip administration of SRIF-AS, no change in serum GH concentration was observed in 2-h-old rats. However, under the same conditions, a significant increase in serum GH was observed in 24-h-old rats and in 2- to 60-day-old rats. The injection of SRIF-AS neither changed basal serum TSH levels during the neonatal development nor in the adult stage. A significant increase in TRH-induced TSH release was observed after the third postnatal day. It is concluded that endogenous SRIF plays a physiological role in GH release by 24 h of age in the rat and that the fall in GH secretion that normally occurs during the first week of life is due to the development of inhibitory mechanisms mediated by hypothalamus SRIF. Additionally the results suggest that the influence of SRIF upon TSH secretion is present before that of TRH.

Aging↗
PubMed1982

Adrenocorticotropin, and corticosterone secretion in Brattleboro rats.

Brattleboro rats which lack endogenous vasopressin have been used to study the role of vasopressin as a corticotropin-releasing factor. Plasma ACTH, beta-endorphin, and corticosterone were measured by RIA in male and female Long-Evans and Brattleboro rats under the following conditions: unstressed, after ether stress, after nicotine injection, and after adrenalectomy. A significant reduction in the ACTH, beta-endorphin, and corticosterone responses to the different experimental procedures was observed in the Brattleboro rats. However, in this strain of rats, a significant increase in the release of all three hormones was obtained, suggesting that vasopressin has only a synergistic role in the regulation of their secretion.

Adrenal Glands↗
PubMed1982

[Demonstration of enkephalins in pheochromocytoma].

Adrenal medulla has recently been shown to contain high concentrations of enkephalin immunoreactive peptides. In the present study, we report the levels of M-ENK and L-ENK in extracts from 6 cases of human pheochromocytoma. The molecular forms of M-ENK have been characterized by gel filtration chromatography and HPLC. mRNA extracted from one tumor has been proved to code for a 80,000 kilo daltons protein containing M-ENK sequence. M-ENK immunoreactive peptides are secreted in the culture medium of dispersed cultured cells of human pheochromocytoma. This secretion is stimulated when nicotine (10(5) M) is added to the medium. However, the level of plasma M-ENK in pheochromocytoma patients is not significantly different from normal patients. Data from Holaday and al. have established that naloxone (an opiate antagonist) has a beneficial role in shock. But the origin and meaning of plasma M-ENK remain to be established.

Adrenal Gland Neoplasms↗
PubMed1981

Effect of neonatal treatment with monosodium glutamate on the secretion of alpha-MSH, beta-endorphin and ACTH in the rat.

Plasma alpha-MSH, beta-endorphin and ACTH were measured at 60 days of age in rats which had been injected during the neonatal period with monosodium glutamate (MSG). Although the arcuate nucleus tuberoinfundibular dopaminergic and cholinergic system was lesioned by the MSG, no change in circulating alpha-MSH, ACTH and corticosterone levels was observed under basal conditions, after ether stress of adrenalectomy. In contrast, a moderate, but significant decrease in plasma beta-endorphin was noticed after MSG treatment.

Adrenalectomy↗
PubMed1980

beta-Endorphin is present in high concentration in the hypophysial portal vessels of rats.

beta-Endorphin-like immunoreactivity (beta-ELI) was measured in hypophysial portal and arterial blood of intact, adrenalectomized and hypophysectomized rats. beta-ELI levels were 61 times higher in the long portal vessels than in the general circulation. Circulating, and especially portal, levels of beta-ELI were significantly increased after adrenalectomy. After removal of the pituitary gland, the mean level of beta-ELI in portal blood was significantly lower than in intact rats. beta-ELI in portal blood displayed the same chromatographic properties as synthetic beta-endorphin.

Adrenalectomy↗
PubMed1980

[Hypothalamic control of ACTH secretion].

The hypothalamic regulation of ACTH secretion has been reviewed. Recent biochemical investigations on corticotropin-releasing factor (CRF) suggest that CRF is present in the hypothalamus under two or more different molecular weight forms, their structure being not elucidated yet. Vasopressin has a CRF-like activity. However, contradictory results have been reported on the role of AVP as a physiological CRF. The synthesis of CRF appears to occur in a large hypothalamic area outside the median eminence. CRF-carrying fibers are thought to pass through the lateral retrochiasmatic area and project on the hypophysial portal vessels at the junction between the pituitary stalk and the median eminence. Conflicting data have been published on the influence of monoamines on ACTH secretion. In the dog, ACTH release is inhibited by the alpha-adrenergic receptors, this effect being not as clearly demonstrated in other species. The stimulation of nicotinic and muscarinic receptors followed by increased ACTH secretion. Glucocorticoids appear to lower ACTH secretion through an action at both the hypothalamic and pituitary levels.

Acetylcholine↗
PubMed1980

[Lipocorticotropic peptides in Cushing's disease: in vitro studies].

The immunologic patterns of 3 human pituitary adenomas of Cushing's disease have been studied after gel exclusion chromatography (Sephadex G-50). The immunologic characteristics were examined with three radioimmunoassays specific for human corticotropin (ACTH), lipotropin (LPH) and beta-endorphin (beta-End). In cell tumor extracts, chromatographic peaks corresponding to beta-LPH, gamma-LPH, beta-End and ACTH were identified. The ACTH/beta-LP-beta-End ratio was 1 in the 3 cases. Additionally, in the 3 cases, a chromatographic peak, partially cross-reacting in the beta-End assay, was eluted after beta-End, thus suggesting the presence of a fragment of the molecule. In 1 case, a peak of large molecular weight material with N- and C-terminal beta-LPH and ACTH immunoreactivity was observed, which corresponded to the precursor material. The release and the effects of various stimuli were studied on dispersed tumor cells in primary culture. The tumor cells had a biphasic basal secretion rate with a rapid increase of ACTH/beta-LPH-beta-End in the culture medium during the first 2 h. Then the release, studied during 2 days, was slower. Chromatographic studies showed that the beta-LPH/beta-End ratio was 0.8 in the cells and 0.3 in the medium, due essentially to the release of beta-End and beta-End-like materials. The cells released ACTH and beta-LPH-beta-End in equimolar ratio after stimulation with arginine vasopressin (AVP). The maximum effect was obtained with 10(-6) M AVP (D50 = 1 10(-9) M). Dibutyryl cyclic AMP (2. 10(-3) M) induced maximal release of ACTH/beta-LPH-beta-End. This stimulation was suppressed by a 48-hour preincubation with dexamethasone (10(-8)-10(-6) M). There was no effect of TRH and LH-RH on cell release. Dopamine (10(-6) M) specifically blocked the release of ACTH/beta-LPH-beta-End in 1 case. These data showed (a) heterogeneity of chromatographic profiles from case to case; (b) the presence of material in the tumor, cell extracts and culture medium corresponding to fragment(s) of beta-End; (c) culture studies demonstrated that tumor cells remain responsive to AVP stimulation and dexamethasone suppression, and (d) the dopamine inhibition of ACTH and beta-End release needs further investigation.

Adenoma↗
PubMedDate not supplied

Peptidylglycine alpha-amidating monooxygenase activity and TRH and CRF biosynthesis. Role of copper.

Carboxy-terminal amidation of biologically active peptides, an important characteristic of more than half of these substances, occurs during the maturation process of peptide precursors. It is catalyzed by peptidylglycine alpha-amidating monooxygenase (PAM), an enzyme that is copper-dependent. We show here that alterations of copper stores in cultured cells from different origins (pancreas and hypothalamus) affect the immunoreactivity of thyrotropin-releasing hormone (TRH) and corticotropin-releasing factor (CRF) (two alpha-amidated peptides). This suggests that copper can affect neuropeptide biosynthesis and may play a role in the endocrine or central nervous system function.

Amino Acid Sequence↗
PubMedDate not supplied

Effect of 41-CRF antiserum on the secretion of ACTH, B-endorphin and alpha-MSH in the rat.

In order to elucidate the physiological role of the 41 amino-acid residue corticotropin-releasing factor (41-CRF) on the secretion of ACTH, B-Endorphin and alpha-MSH, plasma levels of these peptides were measured by radioimmunoassay in intact and adrenalectomized rats, two hours after the injection of either 41-CRF antiserum (CRF-AS) or normal rabbit serum for controls. The administration of CRF-AS strikingly lowered the plasma ACTH levels in both intact and adrenalectomized rats. A statistically significant reduction of plasma levels of B-Endorphin was also observed in the same rats. However, the effect of CRF-AS on B-Endorphin release was less pronounced than the effect on ACTH release. No changes in plasma alpha-MSH levels were observed after passive immunization with CRF-AS. We conclude that, in the rat, 41-CRF plays a physiological role in the regulation of ACTH and B-Endorphin secretion, but is not involved in the regulation of alpha-MSH release from the pituitary gland.

Adrenocorticotropic Hormone↗
PubMedDate not supplied

Influence of endogenous growth hormone-releasing factor (GRF) on the secretion of GH during the perinatal period in the rat.

Passive immunization of pregnant rats with a specific antiserum to rat GRF (GRF-AS) is followed by a decrease in fetal serum GH on the 19th day of gestation. A significant reduction in serum GH is still observed in older fetuses and newborn rats. Pituitary GH content increases in 19- and 20-day-old fetuses after GRF-AS administration to their mothers. These results suggest that endogenous fetal hypothalamic GRF (or placenta GRF) play a physiological role in the secretion of pituitary GH as early as the 19th day of fetal life and may be responsible for the peak of GH release that occurs in fetuses at the end of gestation.

Aging↗
PubMedDate not supplied

[Molecular forms of pituitary and plasma ACTH in physiology and pathology].

Immunoreactive ACTH has been found in human pituitary and plasma under different molecular forms: Big ACTH, intermediate ACTH, ACTH 1-39 and fragments of ACTH. In the literature, there are some controversies especially regarding to the importance of Big ACTH in plasma and tissue. Big ACTH is absent or present in only low amounts in plasma and pituitary extracts from normal subjects. However, the proportion of Big ACTH is very high in tumor extracts and plasma obtained from patients with ectopic ACTH syndrome High concentrations of small ACTH fragments are also present in this syndrome.

Addison Disease↗