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Biomedical subjects

E Castanas

Publications and source records attributed to E Castanas.

68 records · Page 4Linked to original sources

[Effects of electric stimulation of the para-ventricular nucleus on corticotropin function in Long-Evans and Brattleboro rats].

Two peptides have a strong corticotropin releasing factor (CRF) activity: arginine vasopressine (AVP) and a 41-residue peptide (41-CRF). Both peptides are present in high concentration in the PVN of the Rat, a zone of the hypothalamus at which electrical stimulation elicits ACTH release. Since homozygous Brattleboro Rats (Di/Di) congenitally lack endogenous AVP, it was of interest to compare the ACTH and corticosterone release after electrical stimulation of the PVN in Long-Evans (L.E.) and Di/Di Rats. In both L.E. and Di/Di Rats, there is a significant increase in plasma ACTH and corticosterone after electrical stimulation of the PVN. However, corticosterone levels are significantly lower in Di/Di than in L.E. Rats whether the Rats have been stimulated or not. It is concluded that a physiological CRF activity is present in the PVN of Di/Di Rats independently of the CRF like activity of AVP.

Adrenocorticotropic Hormone↗

[Effect of passive immunization with an antiCRF antiserum on the secretion of ACTH in rats].

A peptide with 41-residue having CRF activity both in vivo and in vitro has recently been isolated from ovine hypothalami (41-CRF). Passive immunization of Sprague-Dawley Rats with an antiserum against this peptide is followed by a significant decrease in plasma ACTH and cortisosterone levels under basal conditions as well as after ether-stress and adrenalectomy. These data demonstrate that 41-CRF plays a major role in the physiological regulation of ACTH secretion.

Adrenocorticotropic Hormone↗

[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↗

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↗

[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↗

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↗

Human thyroid cancer: membrane thyrotropin binding and adenylate cyclase activity.

To characterize the relationship of the TSH receptor-adenylate cyclase system to differentiation in human thyroid cancers, adenylate cyclase and TSH binding were studied in membranes from primary and metastatis thyroid carcinomas of varying histological types (n = 33) and normal thyroids (n = 12). Membranes from differentiated carcinomas (n = 23) exhibit wide patient to patient variability; some membranes show entirely normal adenylate cyclase and TSH-binding characteristics, and other membranes exhibit decreased TSH stimulation of adenylate cyclase which is accompanied by either a normal or decrease TSH-binding site concentration. With respect to the TSH-binding site concentration and TSH stimulation of the adenylat cyclase, the well differentiated carcinomas are not significantly different from normal thyroids, whereas the moderately differentiated and the papillary carcinomas are significantly different (P < 0.001 and P < 0.001, respectively). Membranes from undifferentiated carcinomas (n = 5) and those from medullary carcinomas (n = 5) are characterized by an absence of both TSH binding and TSH stimulation of the adenylate cyclase. In conclusion, while a general relationship exists between the impairment of TSH responsiveness and the dedifferentiation process, no pattern of membrane alteration is specific for any histological type.

Adenocarcinoma↗

Reassessment of opioid binding sites in the rat brain.

Opioid binding sites have been characterized pharmacologically in membranes from different areas of the rat brain. Delta, mu and sites belonging to the kappa family (K1, K2, K3) have been detected. Delta sites were more abundant in cortex and striatum, mu sites in striatum and hypothalamus, while kappa binding site concentration was higher in deeper enkephalic structures (brainstem, cerebellum, hypothalamus) and the pituitary gland. A distinct distribution of each subtype of the kappa site was found: kappa 1 sites were higher in the spinal cord, kappa 2 sites in the brainstem and kappa 3 sites in cerebellum. The distribution of delta and kappa sites in the central nervous system was correlated with the distribution of proenkephalin-A derived peptides and precursors, suggesting that these peptides could be their endogenous ligands.

Animals↗

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↗

[Role of cyclic AMP in gastric secretion. Mechanism of action of pentagastrin and cimetidine].

Studies were conducted to explore the effects of pentagastrin, cimetidine, cimetidine with pentagastrin and atropine with pentagastrin, on the gastric acidity and on cAMP accumulation in gastric fundic mucosa in six healthy human beings. Following gastroscopy, gastric juice was collected, and total gastric acidity was measured. Biopsies of fundic mucosa were obtained for estimation of cAMP. All these measurements were taken place before (control) and after the administration of the medicaments. Pentagastrin increased total gastric acidity and cAMP accumulation. Cimetidine decreased both respectively. Combination of cimetidine with pentagastrin and atropine with pentagastrin increased total gastric acidity and cAMP concentration of gastric mucosa. An excellent linear correlation was also found between gastric acidity and fundic mucosal cAMP. These results support the hypothesis of a regulatory role for pentagastrin and cimetidine in total gastric acidity via a cAMP dependent mechanism in gastric mucosa in human. Our findings give a strong indication in Grossman's proposal that the parietal cell has multiple receptors sites.

Adult↗

[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↗