scholarly journals Eph receptors and zonation in the rat adrenal cortex

2008 ◽  
Vol 198 (1) ◽  
pp. 185-191 ◽  
Author(s):  
Caroline H Brennan ◽  
Alexandra Chittka ◽  
Stewart Barker ◽  
Gavin P Vinson
Keyword(s):  
Adrenal Cortex ◽  
Enzyme Inhibitor ◽  
Zona Glomerulosa ◽  
Eph Receptors ◽  
Migration Patterns ◽  
Eph Receptor ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
And Migration

Although the zonation of the adrenal cortex has a clear functional role, the mechanisms that maintain it remain largely conjectural. The concept that an outer proliferative layer gives rise to cells that migrate inwards, adopting sequentially the zona glomerulosa, fasciculata and reticularis phenotypes, has yet to be explained mechanistically. In other tissues, Eph receptor (EphR)/ephrin signalling provides a mechanism for cellular orientation and migration patterns. Real-time PCR and other methods were used to determine the possible role of Eph/ephrin systems in the rat adrenal. mRNA coding for several members of the EphR family was detected, but out of these, EphA2 provided the closest parallel to zonal organisation. In situ hybridisation showed that EphA2 mRNA and EphA protein were predominantly located in the zona glomerulosa. Its transcription closely reflected expected changes in the glomerulosa phenotype, thus it was increased after a low-sodium diet, but decreased by pretreatment with the angiotensin-converting enzyme inhibitor, captopril. It was also decreased by ACTH treatment, but unaffected by betamethasone. mRNA coding for ephrin A1, the major ligand for the EphA receptors, was also detected in the rat adrenal, though changes evoked by the various pretreatments did not clearly reflect the expected changes in zonal function. Because the maintenance of cellular zonation requires clear positional signals within the adrenal cortex, these data support a role for Eph forward and reverse signalling in the maintenance of adrenocortical zonation.

scholarly journals The Role of the Eph Receptor Family in Tumorigenesis

Cancers ◽  
2021 ◽  
Vol 13 (2) ◽  
pp. 206
Author(s):  
Meg Anderton ◽  
Emma van der Meulen ◽  
Melissa J. Blumenthal ◽  
Georgia Schäfer
Keyword(s):  
Kaposi's Sarcoma ◽  
Kaposi’S Sarcoma ◽  
Signalling Pathways ◽  
Cancer Therapies ◽  
Eph Receptors ◽  
Eph Receptor ◽  
Ephrin Ligands ◽  
And Migration ◽  
Receptor Family

The Eph receptor tyrosine kinase family, activated by binding to their cognate ephrin ligands, are important components of signalling pathways involved in animal development. More recently, they have received significant interest due to their involvement in oncogenesis. In most cases, their expression is altered, affecting the likes of cell proliferation and migration. Depending on the context, Eph receptors have the potential to act as both tumour promoters and suppressors in a number of cancers, such as breast cancer, colorectal cancer, lung cancer, prostate cancer, brain cancer and Kaposi’s sarcoma (KS), the latter being intrinsically linked to EphA2 as this is the receptor used for endothelial cell entry by the Kaposi’s sarcoma-associated herpesvirus (KSHV). In addition, EphA2 deregulation is associated with KS, indicating that it has a dual role in this case. Associations between EphA2 sequence variation and KSHV infection/KS progression have been detected, but further work is required to formally establish the links between EphA2 signalling and KS oncogenesis. This review consolidates the available literature of the role of the Eph receptor family, and particularly EphA2, in tumorigenesis, with the aim to develop a better understanding of Eph signalling pathways for potential targeting in novel cancer therapies.

Role of brain serotonergic pathways and hypothalamus in regulation of renin secretion

1987 ◽  
Vol 253 (1) ◽  
pp. R179-R185
Author(s):  
E. Gotoh ◽  
K. Murakami ◽  
T. D. Bahnson ◽  
W. F. Ganong
Keyword(s):  
Plasma Renin ◽  
Dorsal Raphe ◽  
Raphe Nucleus ◽  
Renin Secretion ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Head Up Tilt ◽  
Dorsal Raphé

To investigate the role of brain serotonergic neurons in the regulation of renin secretion, we measured changes in plasma renin activity (PRA), and, in some instances, plasma renin concentration (PRC), plasma angiotensinogen, and plasma adrenocorticotropic hormone (ACTH) in rats with lesions of the dorsal raphe nucleus and lesions of the paraventricular nuclei, dorsomedial nuclei, and ventromedial nuclei of the hypothalamus. We also investigated the effects of p-chloroamphetamine (PCA), immobilization, head-up tilt, and a low-sodium diet in the rats with dorsal raphe, paraventricular, and dorsomedial lesions. Lesions of the dorsal raphe nucleus abolished the increase in PRA produced by PCA but had no effect on the increase produced by immobilization, head-up tilt, and a low-sodium diet. Paraventricular lesions, which abolish the increase in plasma ACTH produced by PCA, immobilization, and head-up tilt, decreased plasma angiotensinogen. The paraventricular lesions abolished the PRA and the PRC responses to PCA and the PRA but not PRC response to immobilization, head-up tilt, and a low-sodium diet. The ventromedial lesions abolished the PRA and PRC responses to PCA and did not reduce plasma angiotensinogen. The data suggest that paraventricular lesions depress angiotensinogen production by the liver and that the paraventricular and ventromedial nuclei are part of the pathway by which serotonergic discharges increase renin secretion. They also suggest that the serotonergic pathway does mediate the increases in renin secretion produced by immobilization, head-up tilt, and a low-sodium diet.

Conclusion

2007 ◽  
Author(s):  
Michael B. Miller
Keyword(s):  
Immigration Policy ◽  
Migration Patterns ◽  
The Core ◽  
Mass Migration ◽  
And Migration

This final chapter offers a conclusion to the overall findings of the journal. It summarises the core factors of mass migration: migration patterns and networks; the role of governments and immigration policy; the importance of steamship emigration agents; the business of migration; and the shifting role of ports and port infrastructures. It concludes by suggesting that maritime and migration historians can further their studies by expanding and exploring one another’s territories.

Control of adrenal cell proliferation by AT1 receptors in response to angiotensin II and low-sodium diet

1999 ◽  
Vol 276 (2) ◽  
pp. E303-E309 ◽  
Author(s):  
Pauline E. McEwan ◽  
Gavin P. Vinson ◽  
Christopher J. Kenyon
Keyword(s):  
Cell Proliferation ◽  
Angiotensin Ii ◽  
Zona Glomerulosa ◽  
Ang Ii ◽  
Adrenal Cell ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Glomerulosa Cells

The effects of angiotensin II (ANG II), the angiotensin type 1 (AT1) receptor antagonist losartan, and low-sodium diet on rat adrenal cell proliferation were studied in vivo with immunocytochemistry. Both ANG II and low-sodium diet increased proliferation of endothelial cells of the zona glomerulosa. Losartan prevented ANG II-induced hyperplasia of glomerulosa cells but not the effects of a low-sodium diet. Glomerulosa cells after ANG II + losartan treatment appeared hypertrophied compared with those of controls. Proliferative effects of ANG II and low-sodium diet in the reticularis were blocked by losartan. No changes were seen in the fasciculata. Proliferation in the medulla was increased with losartan, was decreased by ANG II, but was unaffected by low-sodium diet. In conclusion, 1) cell hypertrophy and proliferation of glomerulosa cells are mediated by AT1 receptor-dependent and -independent processes, 2) proliferation of reticularis cells is controlled by AT1 receptors, and 3) reciprocal control of chromaffin cell proliferation by ANG II may involve indirect AT1-dependent processes.

Role of adrenal renin-angiotensin system in the control of aldosterone secretion in sodium-restricted rats

2000 ◽  
Vol 278 (6) ◽  
pp. E1027-E1030 ◽  
Author(s):  
Giuseppina Mazzocchi ◽  
Ludwik K. Malendowicz ◽  
Anna Markowska ◽  
Giovanna Albertin ◽  
Gastone G. Nussdorfer
Keyword(s):  
Enzyme Inhibitor ◽  
Renin Angiotensin System ◽  
Zona Glomerulosa ◽  
Normal Diet ◽  
Angiotensin Ii Receptor ◽  
Aldosterone Secretion ◽  
Angiotensin System ◽  
Renin Angiotensin

This study examined the effect of the pharmacological manipulation of adrenal renin-angiotensin system (RAS) on aldosterone secretion from in situ perfused adrenals of rats kept on a normal diet and sodium restricted for 14 days. Neither the angiotensin-converting enzyme inhibitor captopril nor the nonselective angiotensin II receptor antagonist saralasin and the AT1 receptor-selective antagonist losartan affected basal aldosterone output in normally fed rats. In contrast, they concentration dependently decreased aldosterone secretion in sodium-restricted animals, with maximal effective concentration ranging from 10− 7 to 10− 6 M. Captopril (10− 6 M), saralasin (10− 6 M), and losartan (10− 7 M) counteracted aldosterone response to 10 mM K+ in sodium-restricted rats but not in normally fed animals. Collectively, these findings provide evidence that adrenal RAS plays a role in the regulation of aldosterone secretion, but only under conditions of prolonged stimulation of zona glomerulosa probably leading to overexpression of adrenal RAS.

Stimulation of aldosterone biosynthesis by sodium sequestration: role of angiotensin II

1982 ◽  
Vol 243 (6) ◽  
pp. E450-E457
Author(s):  
J. Muller ◽  
E. G. Lund ◽  
L. Hofstetter ◽  
D. B. Brunner ◽  
P. Haldy
Keyword(s):  
Angiotensin Ii ◽  
Enzyme Inhibitor ◽  
Zona Glomerulosa ◽  
High Dose ◽  
Converting Enzyme ◽  
Bilateral Nephrectomy ◽  
Stimulatory Action ◽  
Sodium Sequestration ◽  
Stimulation Of

The role of angiotensin II in the stimulation of aldosterone biosynthesis by sodium sequestration in potassium-deficient rats was assessed by experiments involving 1-day angiotensin II infusion, converting enzyme inhibition, and bilateral nephrectomy. In intact rats, only an extremely high dose of exogenous angiotensin II imitated the stimulatory effects of polyethylene glycol-induced edema on the conversions of deoxycorticosterone and corticosterone to 18-hydroxycorticosterone and aldosterone. Treatment with the converting enzyme inhibitor captopril as well as bilateral nephrectomy blocked the aldosterone-stimulating action of edema. This inhibition was prevented by the simultaneous infusion of angiotensin II in captopril-treated rats but not in nephrectomized animals. According to these results, angiotensin II is an essential mediator in the stimulation of aldosterone biosynthesis by sodium sequestration. However, the role of the kidneys appears to be twofold. First, they act through the secretion of renin. In addition, a second yet unknown kidney factor is necessary for a full response of the zona glomerulosa to the stimulatory action of angiotensin II.

Abstract 010: CD44 and CD44+ Cells are Dispensable for the Recruitment of Renin Expressing Cells

Hypertension ◽  
2016 ◽  
Vol 68 (suppl_1) ◽  
Author(s):  
Maria Luisa S Sequeira Lopez ◽  
Brian C Belyea ◽  
Rajwinderjit Kaur ◽  
Silvia Medrano ◽  
R. Ariel Gomez
Keyword(s):  
Inflammatory Process ◽  
Wild Type ◽  
Cell Recruitment ◽  
Qrt Pcr ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Renin Gene ◽  
Kidney Section ◽  
Number Of Cells

In response to a homeostatic stress the number of cells that make renin increases dramatically along the renal arteriolar tree resembling the embryonic pattern. We have shown that this “recruitment” occurs by re-expression of renin in smooth muscle cells that differentiated from embryonic renin cells. A recent study proposed that during recruitment, renal CD44+ mesenchymal stem-like cells can differentiate into juxtaglomerular (JG)-like renin-producing cells. To test such hypothesis, we assessed the distribution and role of CD44+ cells in renin cell recruitment. Mice with homozygous (KO) and heterozygous (het) deletion of CD44 (knockin for LacZ) were treated with low-sodium diet (0.05%) plus captopril (0.5 g/l) for 10 days (n: 9 treated, 7 controls). Body and kidney weights and BP were not different between KO and het mice. BUN and creatinine were significantly increased in both KO and Het treated mice. The number of renin expressing cells in the kidney and circulating renin increased similarly in treated mice (ELISA, untreated: het 131,503 ± 19,319 pg/mL vs KO 84,714 ± 29,065 pg/mL p=0.2517; treated: het 367,850 ± 38,189 pg/mL vs KO 495,120 ± 80,311 pg/mL p=0.2311). Interestingly, immunostaining for CD44 was negative in kidneys of untreated and treated wild type mice. We occasionally observed in CD44-LacZ het or KO mice isolated LacZ positive cells inside the glomeruli (1 or less per sagittal kidney section) and none in the JG area. On the other hand, immunostaining for CD44 on kidney sections of Ren1cKO mice revealed positive cells within perivascular infiltrates. To confirm these results we performed qRT-PCR for CD44 on kidney samples from CD44 het and KO treated, untreated, control, and Ren1cKO mice. CD44 mRNA expression confirmed the histological findings. In summary: 1) CD44 is dispensable for renin expression and recruitment, and 2) CD44+ cells do not contribute to the pool of renin expressing cells in the kidney during basal conditions or in response to a homeostatic stress as previously suggested. However, they do participate in the inflammatory process observed surrounding the vessels in mice with deletion of the renin gene, suggesting that they derived from the circulation and not from the kidney.

Aldosterone response to sodium deprivation and angiotensin II in patients with hypopituitarism

1981 ◽  
Vol 96 (3) ◽  
pp. 361-369 ◽  
Author(s):  
Cornelia Seifert ◽  
Wolfgang Oelkers
Keyword(s):  
Angiotensin Ii ◽  
Pituitary Gland ◽  
Blood Pressure Response ◽  
Normal Subjects ◽  
Zona Glomerulosa ◽  
Sodium Balance ◽  
Sodium Deficiency ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium

Abstract. Unknown pituitary factor(s) apart from ACTH may participate in the regulation of aldosterone (aldo) secretion in man. We investigated whether the 'sensitization' of the zona glomerulosa against angiotensin II (A II) by sodium deficiency was mediated by the pituitary gland. A II was infused in stepwise increasing doses (2, 4, 8 ng/kg/min) into 5 normal subjects (N) and into 8 patients with hypopituitarism (H) before and after 4 days on a low sodium diet. Mean cumulative sodium balance after the low sodium diet was − 145 mm in N and − 165mm in H. Plasma-aldo and aldo-exretion rate on the normal sodium diet were slightly lower in H than in N but rose less than normal during sodium depletion in H. Plasma A II and renin activity on normal sodium were slightly higher in H than in N, but the increase on the low sodium diet was blunted in H. The stimulation of plasmaaldo by A II infusion was similar in both groups on the normal sodium diet. In both groups, the response of P-aldo to A II infusion was greater in the sodium deplete than in the replete state, although 'sensitization' was slightly less marked in H than in N. This may be due to the blunted rise of plasma-A II after sodium loss in H, which may also account for abnormalities in the blood pressure response in the H group. Altogether, the results speak against a direct involvement of the pituitary gland in 'sensitization', but an indirect influence through unexplained abnormalities in renin secretion is possible.

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