Academic literature on the topic 'Peptide effects/adrenal cortex'
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Journal articles on the topic "Peptide effects/adrenal cortex"
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Hinson, JP, and S. Kapas. "Actions of vasoactive intestinal peptide on the rat adrenal zona glomerulosa." Journal of Endocrinology 161, no. 1 (1999): 51–57. http://dx.doi.org/10.1677/joe.0.1610051.
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Previous studies, by this group and others, have shown that vasoactive intestinal peptide (VIP) stimulates aldosterone secretion, and that the actions of VIP on aldosterone secretion by the rat adrenal cortex are blocked by beta adrenergic antagonists, suggesting that VIP may act by the local release of catecholamines. The present studies were designed to test this hypothesis further, by measuring catecholamine release by adrenal capsular tissue in response to VIP stimulation. Using intact capsular tissue it was found that VIP caused a dose-dependent increase in aldosterone secretion, with a concomitant increase in both adrenaline and noradrenaline release. The effects of VIP on aldosterone secretion were inhibited by atenolol, a beta1 adrenergic antagonist, but not by ICI-118,551, a beta2 adrenergic antagonist. Binding studies were carried out to investigate VIP receptors. It was found that adrenal zona glomerulosa tissue from control rats contained specific VIP binding sites (Bmax 853+/-101 fmol/mg protein; Kd 2.26+/-0.45 nmol/l). VIP binding was not displaced by ACTH, angiotensin II or by either of the beta adrenergic antagonists. The response to VIP in adrenals obtained from rats fed a low sodium diet was also investigated. Previous studies have found that adrenals from animals on a low sodium diet exhibit increased responsiveness to VIP. Specific VIP binding sites were identified, although the concentration or affinity of binding sites in the low sodium group was not significantly different from the controls. In the low sodium group VIP was found to increase catecholamine release to the same extent as in the control group, however, in contrast to the control group, the adrenal response to VIP was not altered by adrenergic antagonists in the low sodium group. These data provide strong support for the hypothesis that VIP acts by the local release of catecholamines in adrenal zona glomerulosa tissue in normal animals. It does not appear that VIP acts through the same mechanism in animals maintained on a low sodium diet. The mechanism by which VIP stimulates aldosterone in this group remains to be determined.
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Thomson, LM, S. Kapas, M. Carroll, and JP Hinson. "Autocrine role of adrenomedullin in the human adrenal cortex." Journal of Endocrinology 170, no. 1 (2001): 259–65. http://dx.doi.org/10.1677/joe.0.1700259.
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Previous studies from our laboratory have reported that adrenomedullin is synthesised in rat zona glomerulosa cells. In the present studies, it was found that the human adrenocortical cell line H295R expresses the gene encoding adrenomedullin, and that immunoreactive adrenomedullin is released into the culture medium. Furthermore, it was found that secretion of adrenomedullin is regulated by angiotensin II and forskolin. Studies on the actions of adrenomedullin and calcitonin gene-related peptide (CGRP) revealed a stimulatory effect of adrenomedullin, but not of CGRP, on aldosterone and cortisol secretion. These data suggest that adrenomedullin is not acting by a CGRP receptor-mediated mechanism in the H295R cell line. Adrenomedullin was also found to increase cAMP production, suggesting that in the adrenal, as in other cell types, cAMP is a second messenger for adrenomedullin action. However, the effects of adrenomedullin were not fully mimicked by forskolin, possibly suggesting a role for an additional second messenger. The presence of mRNA encoding both the putative adrenomedullin receptors, L1 and calcitonin receptorlike receptor/receptor-associated modulatory protein 2 (CRLR/RAMP-2), was demonstrated in H295R cells, but RAMP-1 was not detected, suggesting that these cells do not express the CGRPI receptor CRLR/RAMP-1. Taken together, these data have demonstrated that adrenomedullin is synthesised and secreted by H295R cells. The observed rate of adrenomedullin synthesis suggests that this peptide exerts a paracrine/autocrine effect in this adrenocortical cell line, probably acting through a specific adrenomedullin receptor, to stimulate steroidogenesis and increase aldosterone synthase expression.
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Hinson, J. P., L. A. Cameron, and S. Kapas. "Neuropeptide Y modulates the sensitivity of the rat adrenal cortex to stimulation by ACTH." Journal of Endocrinology 145, no. 2 (1995): 283–89. http://dx.doi.org/10.1677/joe.0.1450283.
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Abstract Neuropeptide Y (NPY) has been identified in nerves supplying the adrenal cortex of several mammalian species, although its function in this tissue is unknown. The present studies, employing adrenocortical cells prepared by collagenase digestion, have shown that NPY, in the absence of other stimulants, has no effect on steroid secretion by the rat adrenal over a range of peptide concentrations (10−11 to 10 −6 mol/l). However, in the presence of physiological concentrations of ACTH, which are submaximal for the stimulation of aldosterone secretion, NPY (10−6 mol/l) significantly enhanced the secretion rate of aldosterone by rat zona glomerulosa cells in response to ACTH. This effect was specific to the rat zona glomerulosa as NPY had no effect on the response to ACTH in rat zona fasciculata cells. The effect of NPY appears to be biphasic, however, as NPY significantly attenuated the steroidogenic response to supramaximal ACTH concentrations: in rat zona glomerulosa cells the aldosterone response to 10 −8 mol ACTH/l was significantly inhibited by NPY. The effect of NPY on the ACTH response appeared to be mediated by changes in the cAMP response. NPY had no effect on the steroidogenic response to potassium ions (K+), but enhanced the response to angiotensin II. NPY (10 −6 mol/l) significantly stimulated inositol 1,4,5-trisphosphate (InsP3) production although this concentration of peptide had no effect on steroid secretion. The effects of NPY on InsP3 production were additive with those of angiotensin II. These results suggest that the role of NPY in the adrenal cortex may be to regulate the sensitivity of the zona glomerulosa to peptide stimulation. Journal of Endocrinology (1995) 145, 283–289
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Coll, Anthony P., Martin Fassnacht, Steffen Klammer, et al. "Peripheral administration of the N-terminal pro-opiomelanocortin fragment 1–28 to Pomc−/− mice reduces food intake and weight but does not affect adrenal growth or corticosterone production." Journal of Endocrinology 190, no. 2 (2006): 515–25. http://dx.doi.org/10.1677/joe.1.06749.
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Pro-opiomelanocortin (POMC) is a polypeptide precursor that undergoes extensive processing to yield a range of peptides with biologically diverse functions. POMC-derived ACTH is vital for normal adrenal function and the melanocortin α-MSH plays a key role in appetite control and energy homeostasis. However, the roles of peptide fragments derived from the highly conserved N-terminal region of POMC are less well characterized. We have used mice with a null mutation in the Pomc gene (Pomc−/−) to determine the in vivo effects of synthetic N-terminal 1–28 POMC, which has been shown previously to possess adrenal mitogenic activity. 1–28 POMC (20 μg) given s.c. for 10 days had no effect on the adrenal cortex of Pomc−/− mice, with resultant cortical morphology and plasma corticosterone levels being indistinguishable from sham treatment. Concurrent administration of 1–28 POMC and 1–24 ACTH (30 μg/day) resulted in changes identical to 1–24 ACTH treatment alone, which consisted of upregulation of steroidogenic enzymes, elevation of corticosterone levels, hypertrophy of the zona fasciculate, and regression of the X-zone. However, treatment of corticosterone-depleted Pomc−/− mice with 1–28 POMC reduced cumulative food intake and total body weight. These anorexigenic effects were ameliorated when the peptide was administered to Pomc−/− mice with circulating corticosterone restored either to a low physiological level by corticosterone-supplemented drinking water (CORT) or to a supraphysiological level by concurrent 1–24 ACTH administration. Further, i.c.v. administration of 1–28 POMC to CORT-treated Pomc−/− mice had no effect on food intake or body weight. In wild-type mice, the effects of 1–28 POMC upon food intake and body weight were identical to sham treatment, but 1–28 POMC was able to ameliorate the hyperphagia induced by concurrent 1–24 ACTH treatment. In a mouse model which lacks all endogenous POMC peptides, s.c. treatment with synthetic 1–28 POMC alone can reduce food intake and body weight, but has no impact upon adrenal growth or steroidogenesis.
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Andreis, P. G., G. Neri, T. Prayer-Galetti, et al. "Effects of Adrenomedullin on the Human Adrenal Glands: An in Vitro Study." Journal of Clinical Endocrinology & Metabolism 82, no. 4 (1997): 1167–70. http://dx.doi.org/10.1210/jcem.82.4.3854.
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Abstract Numerous lines of evidence indicate that adrenal medulla exerts a paracrine control on the secretory activity of the cortex by releasing catecholamines and several regulatory peptides. Adrenomedullin (ADM) is contained in adrenal medulla of several mammalian species, including humans. Thus, we investigated whether human ADM1–52 exerts a modulatory action on steroid secretion of human adrenal cortex in vitro. Dispersed adrenocortical cells (obtained from the gland tail deprived of chromaffin cells) and adrenal slices (including both capsule and medulla) were employed. ADM specifically inhibited angiotensin II-stimulated aldosterone secretion of dispersed cells and enhanced basal aldosterone production by adrenal slices, minimal effective concentrations being 10−7 and 10−9 mol/L, respectively. These effects of ADM were suppressed by the CGRP1 receptor antagonist CGRP8–37 (10−5 mol/L). Neither basal and ACTH-stimulated aldosterone secretion of dispersed cells nor agonist-enhanced aldosterone production by adrenal slices were affected by ADM, which also did not alter cortisol secretion of both types of adrenal preparations. ADM (10−6 mol/L) blunted the aldosterone secretagogue action of the Ca2+ ionophore A23187 (10−5 mol/L) on dispersed cells and adrenal slices. Theβ -adrenoceptor antagonist l-alprenolol (10−6 mol/L) suppressed aldosterone response of adrenal slices to 10−7 mol/L isoprenaline and ADM. ADM concentration dependently raised epinephrine and norepinephrine release by adrenal slices, minimal effective concentration being 10−9 mol/L. Collectively, these findings suggest that ADM, acting via the CGRP1 receptor subtype, exerts a direct inhibitory effect on angiotensin II-stimulated aldosterone secretion, which, when the integrity of adrenal tissue is preserved, is overcome and reversed by an indirect stimulatory action, conceivably involving the release of catecholamines by adrenal chromaffin cells.
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Kapas, S., A. Martinez, F. Cuttitta, and JP Hinson. "Local production and action of adrenomedullin in the rat adrenal zona glomerulosa." Journal of Endocrinology 156, no. 3 (1998): 477–84. http://dx.doi.org/10.1677/joe.0.1560477.
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This study was designed to investigate the synthesis and action of adrenomedullin in the rat adrenal gland. The results obtained from in situ hybridization and immunocytochemical studies suggest that adrenomedullin is synthesized not only in the medulla, but also within the zona glomerulosa of the rat adrenal cortex. Findings from in situ hybridization and binding studies also suggested that specific adrenomedullin receptors are expressed in the zona glomerulosa, and that low levels are present in the inner zones of the cortex. The Kd of the zona glomerulosa adrenomedullin receptor (5.5 nmol/l) suggests that it may respond to locally produced adrenomedullin rather than circulating concentrations of the peptide, which are in a lower range. It was found that adrenomedullin acted on zona glomerulosa cells in vitro to stimulate aldosterone release and cAMP formation, but in this tissue did not stimulate inositol phosphate turnover. The effect of adrenomedullin on aldosterone secretion was significantly attenuated by a protein kinase A inhibitor, suggesting that cAMP mediates the effects of adrenomedullin on aldosterone secretion. Adrenomedullin did not significantly affect the response of zona glomerulosa cells to stimulation by either ACTH or angiotensin II. Adrenomedullin did not affect the release of catecholamines, either adrenaline or noradrenaline, by intact adrenal capsular tissue. These data suggest that both adrenomedullin and its specific receptor are expressed in the rat adrenal zona glomerulosa, leading to the hypothesis that adrenomedullin may have an autocrine/paracrine role in the regulation of the rat adrenal zona glomerulosa.
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Hinson, J. P., S. Kapas, C. D. Orford, and G. P. Vinson. "Vasoactive intestinal peptide stimulation of aldosterone secretion by the rat adrenal cortex may be mediated by the local release of catecholamines." Journal of Endocrinology 133, no. 2 (1992): 253–58. http://dx.doi.org/10.1677/joe.0.1330253.
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ABSTRACT The effects of vasoactive intestinal peptide (VIP) on adrenocortical function were investigated using several different preparations of adrenocortical tissue. VIP caused a significant increase in perfusion medium flow rate and in aldosterone and corticosterone secretion by the isolated perfused rat adrenal gland, with a threshold of 1 pmol in 200 μl, but did not affect basal steroid secretion by collagenase-dispersed adrenocortical cells at any concentration used, from 10 pmol/l to 10 μmol/l. The presence of VIP (100 nmol/l) had no significant effect on the response of zona glomerulosa cells to stimulation by ACTH at any concentration. In incubations of intact adrenal capsular tissue, VIP (10 μmol/l) caused a significant stimulation of aldosterone secretion, and also induced a significant release of adrenaline into the incubation medium. Addition of (−)alprenolol (100 nmol/l), a βadrenergic antagonist, to the incubation medium significantly attenuated the response of capsular tissue to VIP. It is concluded that the effects of VIP on aldosterone, which are only seen when the architecture of the zona glomerulosa is preserved, may be mediated by the local release of adrenaline. Journal of Endocrinology (1992) 133, 253–258
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Karteris, Emmanouil, Rachel J. Machado, Jing Chen, Sevasti Zervou, Edward W. Hillhouse, and Harpal S. Randeva. "Food deprivation differentially modulates orexin receptor expression and signaling in rat hypothalamus and adrenal cortex." American Journal of Physiology-Endocrinology and Metabolism 288, no. 6 (2005): E1089—E1100. http://dx.doi.org/10.1152/ajpendo.00351.2004.
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Although starvation-induced biochemical and metabolic changes are perceived by the hypothalamus, the adrenal gland plays a key role in the integration of metabolic activity and energy balance, implicating feeding as a major synchronizer of rhythms in the hypothalamic-pituitary-adrenal (HPA) axis. Given that orexins are involved in regulating food intake and activating the HPA axis, we hypothesized that food deprivation, an acute challenge to the systems that regulate energy balance, should elicit changes in orexin receptor signaling at the hypothalamic and adrenal levels. Food deprivation induced orexin type 1 (OX1R) and 2 (OX2R) receptors at mRNA and protein levels in the hypothalamus, in addition to a fivefold increase in prepro-orexin mRNA. Cleaved peptides OR-A and OR-B are also elevated at the protein level. Interestingly, adrenal OX1R and OX2R levels were significantly reduced in food-deprived animals, whereas there was no expression of prepro-orexin in the adrenal gland in either state. Food deprivation exerted a differential effect on OXR-G protein coupling. In the hypothalamus of food deprived rats compared with controls, a significant increase in coupling of orexin receptors to Gq, Gs, and Go was demonstrated, whereas coupling to Gi was relatively less. However, in the adrenal cortex of the food-deprived animal, there was decreased coupling of orexin receptors to Gs, Go, and Gq and increased coupling to Gi. Subsequent second-messenger studies (cAMP/IP3) have supported these findings. Our data indicate that food deprivation has differential effects on orexin receptor expression and their signaling characteristics at the hypothalamic and adrenocortical levels. These findings suggest orexins as potential metabolic regulators within the HPA axis both centrally and peripherally.
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Delarue, C., JM Conlon, I. Remy-Jouet, A. Fournier, and H. Vaudry. "Endothelins as local activators of adrenocortical cells." Journal of Molecular Endocrinology 32, no. 1 (2004): 1–7. http://dx.doi.org/10.1677/jme.0.0320001.
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Besides the classical corticotropic hormones, ACTH and angiotensin II, various regulatory peptides produced by the adrenal gland are thought to participate in the control of corticosteroid secretion. Here, we review the evidence that endothelins (ETs) synthesized within the adrenal cortex may act as autocrine and/or paracrine factors to regulate adrenocortical cell activity. The expression of ETs has been detected in normal, hyperplastic and neoplastic adrenocortical cells. The occurrence of ET receptors has been described in the different zones of the cortex. ETs stimulate the secretion of both glucocorticoids and mineralocorticoids, and modulate the proliferation of adrenocortical cells. The effects of ETs on steroidogenic cells are mediated through the activation of various signaling mechanisms including stimulation of phospholipase C, phospholipase A2 and adenylyl cyclase activity, as well as calcium influx through plasma channels. These observations suggest that locally produced ETs may play an important role in the regulation of corticosteroid secretion and in the control of mitogenesis in normal and tumoral adrenocortical cells.
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Giuliani, Luisa, Livia Lenzini, Michele Antonello, et al. "Expression and Functional Role of Urotensin-II and Its Receptor in the Adrenal Cortex and Medulla: Novel Insights for the Pathophysiology of Primary Aldosteronism." Journal of Clinical Endocrinology & Metabolism 94, no. 2 (2009): 684–90. http://dx.doi.org/10.1210/jc.2008-1131.
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Abstract Context: The involvement of urotensin II, a vasoactive peptide acting via the G protein-coupled urotensin II receptor, in arterial hypertension remains contentious. Objective: We investigated the expression of urotensin II and urotensin II receptor in adrenocortical and adrenomedullary tumors and the functional effects of urotensin II receptor activation. Design: The expression of urotensin II and urotensin II receptor was measured by real time RT-PCR in aldosterone-producing adenoma (n = 22) and pheochromocytoma (n = 10), using histologically normal adrenocortical (n = 6) and normal adrenomedullary (n = 5) tissue as control. Urotensin II peptide and urotensin II receptor protein were investigated with immunohistochemistry and immunoblotting. To identify urotensin II-related and urotensin II receptor-related pathways, a whole transcriptome analysis was used. The adrenocortical effects of urotensin II receptor activation were also assessed by urotensin II infusion with/without the urotensin II receptor antagonist palosuran in rats. Results: Urotensin II was more expressed in pheochromocytoma than in aldosterone-producing adenoma tissue; the opposite was seen for the urotensin II receptor expression. Urotensin II receptor activation in vivo in rats enhanced (by 182 ± 9%; P < 0.007) the adrenocortical expression of immunoreactive aldosterone synthase. Conclusions: Urotensin II is a putative mediator of the effects of the adrenal medulla and pheochromocytoma on the adrenocortical zona glomerulosa. This pathophysiological link might account for the reported causal relationship between pheochromocytoma and primary aldosteronism.
Dissertations / Theses on the topic "Peptide effects/adrenal cortex"
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Hansell, D. J. "Action of ACTH peptides on the adrenal gland." Thesis, University of Oxford, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.233492.
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Dunn, Stacey Leanne. "Fetal growth restriction : effects on the adrenal cortex in postnatal lambs /." Title page and abstract only, 2004. http://web4.library.adelaide.edu.au/theses/09SB/09sbd9231.pdf.
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Supornsilchai, Vichit. "Effects of endocrine disruptors on adrenocortical and leydig cell steroidogenesis /." Stockholm : Karolinska institutet, 2007. http://diss.kib.ki.se/2007/978-91-7357-276-7/.
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MacAuley, Iain Alasdair Somerled. "An analysis of the effects of oncogenes and growth factors on rat adrenal cortex cells." Thesis, University of British Columbia, 1987. http://hdl.handle.net/2429/27438.
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The process of oncogenic transformation in vitro has been examined in an attempt to define the molecular mechanisms of carcinogenesis. Transformation in Ki-MSV-infected rat adrenal cortex cells appears to be a multistep process (Auersperg et al., 1981), as does the process of transformation in other nonestablished cells (Land et at., 1983b). The Ki-MSV-infected adrenal cortex cells initially express a partially transformed phenotype and after further passaging progress to a highly transformed phenotype (Calderwood and Auersperg, 1984). Examination of Ki-MSV-infected adrenal cortex cells indicated that progression to a highly transformed phenotype could occur in the absence of significant changes in the level of the expression of the viral ras oncogene. These results indicated that an oncogenically activated ras gene could be expressed in these nonestablished cells in the absence of transformation.
Since ras and myc cooperate to transform primary fibroblasts the effect of the co-introduction of myc on Ki-MSV-induced transformation of adrenal cortex cells was examined. It could be demonstrated that myc and ras cooperate to transform the adrenal cortex cells more efficiently than either oncogene alone, but that the infected cultures initially only express some of the phenotypes associated with transformation. The appearance of a fully transformed phenotype, as monitored by growth in soft agar, was not expressed until several passages after infection. An analysis of the Ki-MSV/MMCV-infected cultures indicated that some of the phenotypes associated with activated oncogenes in immortalized cell lines appeared to be suppressed in the coinfected adrenal cortex cells. Transformation by ras and myc appears to require a further cellular change resulting in a loss of the suppression of oncogene action. The emergence of transformed cultures from the Ki-MSV-infected rat adrenal cortex cells was correlated with the reduced expression of a novel ras-related protein of 27000 Mr.
Transformation induced by src and myc was also examined. These two oncogenes appeared to cooperate in a two step pathway of transformation that was not susceptible to cellular suppression. The transformed phenotype did not appear to be entirely free of external influence as the growth rate of the transformed cells could be modified by culture conditions. The ability of myc to cooperate with src and ras in the transformation of the early passage adrenal cortex cells provides further support for mutistep carcinogenesis.
The effect of oncogenes on steroidogenesis was examined in the Y-1 adrenocortical tumour cell line. The effect of the virally borne oncogenes on growth and morphology of the Y-1 cells was relatively subtle. The oncogenes appear to stimulate the production of fluorogenic steroids, each in a distinct fashion. A model of transformation can be derived in which the roles of the oncogenes and their interaction with the cell can be evaluated. The differences in the pathways of transformation for the two combinations of oncogenes illustrates the potential complexity of the transformation process and provides an in vitro model system for further study.<br>Science, Faculty of<br>Microbiology and Immunology, Department of<br>Graduate
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Bertke, Alexander. "Social Buffering By Unfamiliar Adult Males in Periadolescent Guinea Pigs: The Effects on HPA Axis Activity And Fos Induction In The Medial Prefrontal Cortex." Wright State University / OhioLINK, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=wright1559558966039455.
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Leboulenger, François. "Contribution à l'étude de l'activité de la corticosurrénale des amphibiens anoures, une glande endocrine sous contrôle multifactoriel." Rouen, 1986. http://www.theses.fr/1986ROUES027.
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Mise en évidence des fluctuations saisonnières et journalières des taux circulants de corticostéroïdes. Analyse des paramètres de la réponse corticosurrénalienne à l'ACTH et à différents peptides issus de la maturation de la proopiomélanocortine. Mise en évidence de la co-localisation du VIP et de peptides opiacés dans les granules de sécrétion des cellules chromaffines, rôle de ces peptides dans la stimulation de la stéroïdogenèse. Structure de la proenképhaline A d'amphibien. Rôle de l'acétylcholine via des récepteurs muscariniques utilisant les prostaglandines comme second messager
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Costa, Marcia Helena Soares. "Estudo da expressão dos receptores do peptídeo insulinotrópico dependente de glicose (GIPR) e do hormônio luteinizante (LHCGR) em tumores e hiperplasias do córtex adrenal." Universidade de São Paulo, 2007. http://www.teses.usp.br/teses/disponiveis/5/5135/tde-11092007-134837/.
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Introdução: Os receptores do peptídeo insulinotrópico dependente de glicose (GIPR) e do hormônio luteinizante (LHCGR) são receptores acoplados à proteína G com amplo padrão de expressão tecidual. A expressão anômala destes receptores tem sido descrita em casos de hiperplasia adrenal macronodular independente de ACTH (AIMAH) e em alguns adenomas, resultando em aumento da secreção hormonal (cortisol, andrógenos e aldosterona) pelo cortex adrenal. O papel destes receptores em outras formas de hiperplasia, como a doença adrenocortical nodular pigmentosa primária (PPNAD), aumento da adrenal associado à neoplasia endócrina múltipla tipo 1 (MEN1), e em carcinoma do córtex adrenal tem sido pouco investigado; sendo assim, considera-se relevante estudar a expressão destes receptores nos pacientes com tumores adrenocorticais esporádicos, nos pacientes com AIMAH, PPNAD e aumento adrenal associado à MEN1. Objetivos: 1) Caracterização molecular dos casos de neoplasia endócrina múltipla tipo 1 e PPNAD: pesquisa de mutações dos genes MEN1 e PRKAR1A e análise da perda de heterozigose (LOH) destes genes no tecido adrenal destes pacientes. 2) Quantificar a expressão do GIPR e do LHCGR em tecido adrenocortical normal, tumoral, hiperplásico e correlacionar a expressão destes com a classificação histológica dos tumores adrenocorticais. Pacientes: 55 pacientes (30 adultos) com tumores adrenocorticais (37 adenomas e 18 carcinomas); 7 pacientes com AIMAH, 4 com MEN1, 1 com PPNAD e tecidos controles (adrenal; testículo e pâncreas). Métodos: extração de DNA genômico, RNA e síntese de DNA complementar (cDNA); amplificação por PCR das regiões codificadoras dos genes MEN1 e PRKAR1A seguida por seqüenciamento automático. Pesquisa de LOH pela amplificação de microssatélites por PCR e análise pelo programa GeneScan. Quantificação da expressão do GIPR e do LHCGR por PCR em tempo real pelo método TaqMan e estudo de imunohistoquímica para GIPR nos tumores adrenocorticais. Resultados: identificação de 3 mutações (893+ 1G>A, W183X e A68fsX118) e dois polimorfirmos (S145S e D418D) no gene MEN1 e uma mutação (Y21X) no PRKAR1A. Ausência de LOH nos tecidos adrenais estudados. A expressão do GIPR e do LHCGR foi identificada em tecidos adrenais normais, tumorais e hiperplásicos. O nível de expressão do GIPR foi mais elevado nos tumores adrenocorticais malignos que nos benignos tanto no grupo pediátrico (mediana= 18,1 e 4,6, respectivamente; p <0,05), quanto no grupo adulto (mediana = 4,8 e 1,3 respectivamente; p <0,001). O nível de expressão do LHCGR, no grupo pediátrico, foi elevado tanto nos tumores benignos quanto nos malignos (mediana= 6,4 e 4,3, respectivamente). No grupo adulto os níveis de expressão deste receptor foram extremamente baixos nos tumores malignos em relação aos benignos (mediana= 0,06 e 2,3, respectivamente; p <0,001). A imunohistoquímica para o GIPR foi variável e não correlacionada à expressão do gene GIPR. Não houve diferença nos níveis de expressão do GIPR e do LHCGR nas hiperplasias do córtex adrenal. Conclusões: a presença de LOH e mutação em heterozigose composta do gene MEN1 e do PRKAR1A foram afastadas como mecanismos responsáveis pelo aumento adrenal tanto nos pacientes com MEN1 como no paciente com PPNAD. A hiperexpressão de GIPR está associada a malignidade nos tumores adrenocorticais nos grupos adulto e pediátrico e a baixa expressão de LHCGR está associada a malignidade nos tumores adrenocorticais somente no grupo adulto.<br>Introduction: The glucose- dependent insulinotropic peptide receptor (GIPR) and luteinizing hormone receptor (LHCGR) are G-protein coupled receptors with a wide tissue expression pattern. The aberrant expression of these receptors has been described in cases of ACTH-independent macronodular adrenal hyperplasia (AIMAH) and in some adenomas, resulting in the increase of adrenal cortex hormonal secretion (cortisol, androgens and aldosterone). The role of these receptors in other forms of adrenocortical hyperplasia, such as primary pigmented nodular adrenocortical disease (PPNAD), adrenal enlargement associated with multiple endocrine neoplasia type 1 (MEN1), and adrenocortical carcinoma has been scarcely investigated. Thus, the study of the expression of these receptors in patients with sporadical adrenocortical tumors, AIMAH, PPNAD and adrenal enlargement associated to MEN1 was considered important. Objectives: 1) Molecular study in patients with multiple endocrine neoplasia type 1 and PPNAD: mutation screening of MEN1 and PRKAR1A genes and analysis of the loss of heterozygosis (LOH) of these genes in the adrenal lesions of these patients. 2) To quantify the GIPR and LHCGR expression, in normal, tumor and hyperplasic tissue and to correlate the expression of these receptors with the adrenocortical tumor histology. Patients: 55 patients (30 adults) with adrenocortical tumors (37 adenomas and 18 carcinomas); 7 patients with AIMAH, 4 with MEN1, 1 with PPNAD and control tissue (adrenal, testis and pancreas). Methods: Extraction of genomic DNA, RNA and synthesis of complementary DNA (cDNA); PCR-amplification of the coding regions of MEN1 and PRKAR1A, followed by direct sequencing. LOH study using polymorphic marker amplification by PCR and GeneScan software analysis. Quantification of GIPR and LHCGR expression using realtime PCR -TaqMan method and GIPR immunohistochemistry study in adrenocortical tumors. Results: Identification of 3 mutations (893+ 1G>A, W183X and A68fsX118) and two polymorphic alterations (S145S and D418D) in MEN1 and a mutation (Y21X) in the PRKAR1A gene; LOH was not identified in adrenal tissue. The GIPR and LHCGR expression was identified in normal, tumor and hyperplasic adrenal tissues; the GIPR expression level was more elevated in malignant tumors compared to benign tumors in pediatric (median = 18.1 and 4.6, respectively; p <0.05) and adult patients (median = 4.8 and 1.3 respectively; p <0.001). The LHCGR expression in pediatric patients was elevated in benign as well as in malignant tumors (median = 6.4 and 4.3, respectively). In the adult group, the expression level of these receptors was extremely low in malignant tumors in relation to benign ones (median = 0.06 and 2.3, respectively; p <0.001). The GIPR immunohistochemistry was variable and did not correlate with GIPR gene expression. No difference between GIPR and LHCGR expression levels was observed in the different forms of hyperplasia. Conclusions: The presence of LOH and mutations in compound heterozygosis of MEN1 and PRKAR1A genes were ruled out as the mechanisms responsible for the adrenal enlargement in patients with multiple endocrine neoplasia type 1. GIPR overexpression is associated with malignant adrenocortical tumors in the adult and pediatric patients and low LHCGR expression is associated with malignant adrenocortical tumors only in the adult patients.
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Khan, Tanweera S. "New Diagnostic and Therapeutic Approaches in Adrenocortical Cancer." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2004. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-4243.
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Netchitailo, Pierre. "La corticostéroïdogénèse chez un amphibien anoure : mécanismes intracellulaires et contrôle multifactoriel." Rouen, 1987. http://www.theses.fr/1987ROUES037.
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Zhao, Huifang. "Improved Methods of Sepsis Case Identification and the Effects of Treatment with Low Dose Steroids: A Dissertation." eScholarship@UMMS, 2011. https://escholarship.umassmed.edu/gsbs_diss/529.
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Sepsis is the leading cause of death among critically ill patients and the 10th most common cause of death overall in the United States. The mortality rates increase with severity of the disease, ranging from 15% for sepsis to 60% for septic shock. Patient with sepsis can present varied clinical symptoms depending on the personal predisposition, causal microorganism, organ system involved, and disease severity. To facilitate sepsis diagnosis, the first sepsis consensus definitions was published in 1991 and then updated in 2001. Early recognition of a sepsis patient followed with timely and appropriate treatment and management strategies have been shown to significantly reduce sepsis-related mortality, and allows care to be provided at lower costs. Despite the rapid progress in the knowledge of pathophysiological mechanisms of sepsis and its treatment in the last two decades, identifying patient with sepsis and therapeutic approaches to sepsis and its complications remains challenging to critical care clinicians. Hence, the objectives of this thesis were to 1) evaluate the test characteristics of the two sepsis consensus definitions and delineate the differences in patient profile among patients meeting or not meeting sepsis definitions; 2) determine the relationship between the changes in several physiological parameters before sepsis onset and sepsis, and to determine whether these parameters could be used to identify sepsis in critically ill adults; 3) evaluate the effect of corticosteroids therapy on patient mortality.
Data used in this thesis were prospectively collected from an electronic medical record system for all the adult patients admitted into the seven critical care units (ICUs) in a tertiary medical center. Besides analyzing data at the ICU stay level, we investigated patient information in various time frames, including 24-hour, 12-hour, and 6-hour time windows.
In the first study of this thesis, the 1991 sepsis definition was found to have a high sensitivity of 94.6%, but a low specificity of 61.0%. The 2001 sepsis definition had a slightly increased sensitivity but a decreased specificity, which was 96.9% and 58.3%, respectively. The areas under the ROC curve for the two consensus definitions were similar, but less than optimal. The sensitivity and area under the ROC curve of both definitions were lower at the 24-hour time window level than those of the unit stay level, though the specificity increased slightly. At the time window level, the 1991 definitions performed slightly better than the 2001 definition.
In the second study, minimum systolic blood pressure performed the best, followed by maximum respiratory rate in discriminating sepsis patients from SIRS patients. Maximum heart rate and maximum respiratory rate can differentiate sepsis patients from non-SIRS patients fairly well. The area under ROC of the combination of five physiological parameters was 0.74 and 0.90 for comparing sepsis to non-infectious SIRS patients and comparing sepsis to non-SIRS patients, respectively. Parameters typically performed better in 24-hour windows compared to 6-hour or 12-hour windows.
In the third study, significantly increased hospital mortality and ICU mortality were observed in the group treated with low-dose corticosteroids than the control group based on the propensity score matched comparisons, and multivariate logistic regression analyses after adjustment for propensity score alone, covariates, or propensity score (in deciles) and covariates.
This thesis advances the existing knowledge by systemically evaluating the test characteristics for the 1991 and 2001 sepsis consensus definitions, delineating physiological signs and symptoms of deterioration in the preceding 24 hours prior to sepsis onset, assessing the prediction performances of single or combined physiological parameters, and examining the use of corticosteroids treatment and survival among septic shock patients. In addition, this thesis sets an innovative example on how to use data from electronic medical records as these surveillance systems are becoming increasingly popular. The results of these studies suggest that a more parsimonious set of definitional criteria for sepsis diagnosis are needed to improve sepsis case identification. In addition, continuously monitored physiological parameters could help to identify patients who show signs of deterioration prior to developing sepsis. Last but not least, caution should be used when considering a recommendation on the use of low dose corticosteroids in clinical practice guidelines for the management of sepsis.
Books on the topic "Peptide effects/adrenal cortex"
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Yuuki, Inoue, and Watanabe Kouki, eds. Adverse effects of steroids. Nova Science Publishers, 2008.
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(Editor), Philip W. Harvey, David Everett (Editor), and Christopher Springall (Editor), eds. Adrenal Toxicology (Target Organ Toxicology Series). Informa Healthcare, 2008.
Find full textBook chapters on the topic "Peptide effects/adrenal cortex"
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Mulrow, Patrick J., Roberto Franco-Saenz, K. Atarashi, Masao Takagi, and Mari Takagi. "Effect of Atrial Peptides on the Adrenal Cortex." In Atrial Hormones and Other Natriuretic Factors. Springer New York, 1987. http://dx.doi.org/10.1007/978-1-4614-7529-3_9.
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Höllt, V., and G. Horn. "Nicotine Induces Opioid Peptide Gene Expression in Hypothalamus and Adrenal Medulla of Rats." In Effects of Nicotine on Biological Systems. Birkhäuser Basel, 1991. http://dx.doi.org/10.1007/978-3-0348-7457-1_38.
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Kochakian, Charles D. "The Effects on Enzymes of Adrenal Cortex, Diet, Œstrogens, and Experimental Diabetes." In Ciba Foundation Symposium - Steroid Hormones and Enzymes (Book II of Colloquia on Endocrinology, Vol. 1). John Wiley & Sons, Ltd., 2008. http://dx.doi.org/10.1002/9780470718742.ch12.
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Bergenstal, D. M., Charles Huggins, and Thomas L.-Y. Dao. "Metabolic Effects of Adrenalectomy in Man." In Ciba Foundation Symposium - The Human Adrenal Cortex (Book II of Colloquia on Endocrinology, Vol. 8). John Wiley & Sons, Ltd., 2008. http://dx.doi.org/10.1002/9780470715215.ch9.
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Mach, R. S., and J. Fabre. "Clinical and Metabolic Effects of Aldosterone." In Ciba Foundation Symposium - The Human Adrenal Cortex (Book II of Colloquia on Endocrinology, Vol. 8). John Wiley & Sons, Ltd., 2008. http://dx.doi.org/10.1002/9780470715215.ch6.
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Miyamoto, Hirokuni, Fumiko Mitani, Kuniaki Mukai, and Yuzuru Ishimura. "Effects of ACTH and Angiotensin II on the Novel Cell Layer Without Corticosteroid-Synthesizing Activity in Rat Adrenal Cortex." In Oxygen Homeostasis and Its Dynamics. Springer Japan, 1998. http://dx.doi.org/10.1007/978-4-431-68476-3_29.
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Sherlock, Mark, and Mark Gurnell. "Disorders of the adrenal cortex." In Oxford Textbook of Medicine, edited by Mark Gurnell. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198746690.003.0249.
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Three classes of steroid hormone are produced by the adrenal cortex after uptake of precursor cholesterol from the plasma—mineralocorticoids, glucocorticoids, and sex steroids—with classical endocrine feedback loops controlling their secretion. Glucocorticoids have more diverse and extensive roles than mineralocorticoids, regulating sodium and water homeostasis, glucose and carbohydrate metabolism, inflammation, and stress. These effects are mediated by the interaction of cortisol with ubiquitous glucocorticoid receptors, and the induction or repression of target gene transcription (via glucocorticoid response elements, GREs). Adrenocortical diseases are relatively uncommon, but they have detrimental clinical consequences and can be treated effectively. Hormonal deficiency or excess is usually the result of abnormal secretion.
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Auchus, Richard J., and Keith L. Parker. "The Adrenal Glands." In Textbook of Endocrine Physiology. Oxford University Press, 2011. http://dx.doi.org/10.1093/oso/9780199744121.003.0016.
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The basic function of the adrenal glands is to protect the organism against acute and chronic stress, a concept popularized as the fight-or-flight response for the medulla and as the alarm reaction for the cortex. The steroid hormones of the cortex and the catecholamines of the medulla probably developed as protection against immediate stress or injury and more prolonged deprivation of food and water. In acute stress, catecholamines mobilize glucose and fatty acids for energy and prepare the heart, lungs, and muscles for action, while glucocorticoids protect against overreactions from the body’s responses to stress. In the more chronic stress of food and fluid deprivation, adrenocortical steroid hormones stimulate gluconeogenesis to maintain the supply of glucose and increase sodium reabsorption to maintain body fluid volume. Based on the widespread effects of its secreted products in multiple tissues, adrenal dysfunction is associated with protean manifestations. Diseases associated with adrenocortical hypofunction are relatively rare, while those associated with adrenocortical hyperfunction are slightly more common. However, both of these conditions are life threatening if untreated, and a high index of suspicion must therefore be maintained. Subtle increases in cortisol secretion or tissue sensitivity to glucocorticoids may be involved in many of the devastating effects of chronic stress, including visceral obesity, hypertension, diabetes mellitus, dyslipidemia, infertility, and depression. Moreover, exogenous glucocorticoids are widely used to treat numerous diseases and, when used in supraphysiological doses, can induce all of the manifestations of glucocorticoid excess. Perhaps because the adrenal medulla accounts for only 10 % of total sympathetic nervous activation, we can live quite well without it, and syndromes due to hypofunction are not clinically significant. However, conditions of excess catecholamine output due to tumors called pheochromocytomas are a rare but potentially life-threatening cause of secondary hypertension.
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Ziegler, CG, JW Brown, AV Schally, et al. "Neuropeptide Hormone Receptor Expression in Human Adrenal Tumors and Cell Lines: Antiproliferative Effects of Peptide Analogues." In The Endocrine Society's 92nd Annual Meeting, June 19–22, 2010 - San Diego. Endocrine Society, 2010. http://dx.doi.org/10.1210/endo-meetings.2010.part1.p2.p1-65.
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McCarty, Richard. "Stress-Sensitive Brain Circuits." In Stress and Mental Disorders: Insights from Animal Models. Oxford University Press, 2020. http://dx.doi.org/10.1093/med-psych/9780190697266.003.0005.
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A series of forebrain, midbrain, and brainstem nuclei exert stimulatory or inhibitory effects on sympathetic outflow from the intermediolateral cell column in thoracic and lumbar areas of the spinal cord. Some of these brain areas contain cell bodies that serve as command neurons that can simultaneously activate sympathetic outflow to multiple target tissues. CRF-containing cell bodies in the paraventricular nuclei receive multiple direct and indirect inputs from various brain areas that participate in the regulation of the HPA axis. Hormones of the adrenal cortex have been shown to exert damaging structural effects on the structure of neurons in the hippocampus and amygdala. The immune system is stress-responsive, and circulating immune cells and proinflammatory cytokines are able to penetrate the blood-brain barrier during exposure to stressors. Brain microglia appear to serve as neuroimmune sensors of stress. Optogenetic and chemogenetic techniques have been essential tools in probing the functions of stress-responsive brain circuits and their impact on behavior.
Conference papers on the topic "Peptide effects/adrenal cortex"
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Tanable, A., Y. Yatomi, T. Ohashi, H. Oka, T. Kariya, and S. Kume. "EFFECTS OF HUMAN ATRIAL NATRIURETIC PEPTIDES ON SECRETION REACTION IN HUMAN PLATELETS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644873.
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Human atrial natriuretic peptide (h-ANP) has vasodilating and natriuretic properties, and inhibits smooth muscle contraction, renal renin secretion and adrenal aldosterone release. Although Schiffrin has reported that human platelets have receptors for ANP, its effects in platelets are not established in vivo. We therefore investigated the influence of h-ANP on secretion reaction in human platelets. Eight healthy subjects, males, aged 20 to 24 years, donated blood for the study. Citrated platelet-rich plasma (PRP) was incubated with or without h-ANP at 37 C for 2.5 minutes. The samples of 0.5 ml PRP then used to measure ADP induced aggregation, ATP release reaction and C-serotonin release reaction. H-ANP, at concentration of 1x10 -6M, decreased ADP induced aggregation (after h-ANP: 77.4±9.7 % of control aggregation), and inhibited ATP release reaction (after h-ANP: 31.8±13.1%). Serotonin releasereaction induced by ADP was also inhibited ( control: 15.3±2.2%, after h-ANP: 8.3±0.5 %). The inhibitory effect of h-ANP on aggregation and secretion reaction was maximal by 3 minutes. These data suggest that h-ANP inhibits secretion reaction in human platelets.