scholarly journals Regulation of Aldosterone Synthase Cytochrome P450 (CYP11.BETA.2) and 11.BETA.-Hydroxylase Cytochrome P450 (CYP11B1) Expression in Rat Adrenal Zona Glomerulosa Cells by Low Sodium Diet and Angiotensin II Receptor Antagonists.

1997 ◽  
Vol 20 (9) ◽  
pp. 962-968 ◽  
Author(s):  
Motoharu KAKIKI ◽  
Ken-ichirou MOROHASHI ◽  
Masatoshi NOMURA ◽  
Tsuneo OMURA ◽  
Toru HORIE
Keyword(s):  
Cytochrome P450 ◽  
Angiotensin Ii ◽  
Zona Glomerulosa ◽  
Angiotensin Ii Receptor ◽  
Angiotensin Ii Receptor Antagonists ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Glomerulosa Cells ◽  
Beta 2 ◽  
Zona Glomerulosa Cells

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.

The properties of adrenal zona glomerulosa cells after purification by gravitational sedimentation

1974 ◽  
Vol 185 (1081) ◽  
pp. 375-407 ◽  
Keyword(s):  
Angiotensin Ii ◽  
Cyclic Amp ◽  
Microscopic Examination ◽  
Zona Glomerulosa ◽  
Maximal Response ◽  
Zona Fasciculata ◽  
Gravitational Sedimentation ◽  
Rat Adrenals ◽  
Glomerulosa Cells ◽  
Zona Glomerulosa Cells

The densities of latex spheres and biological cells can be reliably determined from their sedimentation rate in an albumin gradient under unit gravitational force. The densities of zona glomerulosa and fasciculata cells of rat adrenals were found to be 1.072 ± 0.004 and 1.040 ± 0.001 respectively. Purified zona glomerulosa cells of rat adrenals can be prepared by gravitational sedimentation of dispersed cells from capsule strippings of the gland, which originally contain 3 to10% zona fasciculata contamination. Electron and phase microscopic examination of the sedimented glomerulosa cells and their steroidogenic response to ACTH and cyclic AMP indicate that they are reasonably free of contamination from zona fasciculata cells. Electron microscopic examination of the purified glomerulosa cells indicates that most of them are reasonably normal in structure. Their basal production of corticosterone is decreased after sedimentation. However, their maximal response of corticosterone output to serotonin and potassium and their response to all potassium concentrations is not significantly altered, indicating normal function for the cells producing steroids. Their maximal responses to ACTH, valine angiotensin II and cyclic AMP are decreased, but, at the doses used, steroidogenesis by the zona fasciculata contamination in the unfractionated preparation would be stimulated by these substances. Purified zona glomerulosa cells have about the same maximal response of corticosterone output (about twofold) to potassium, valine and isoleucine angiotensin II, serotonin and ACTH. The maximal response of the purified zona glomerulosa cells to cyclic AMP is similar to that elicited by valine and isoleucine angiotensin II, potassium, serotonin or ACTH. This indicates that if these stimuli act by increasing cyclic AMP output, then the maximal response of corticosterone output (about twofold) is defined by the limited response of the biosynthetic pathways to cyclic AMP.

Internalisation of the type I angiotensin II receptor (ATI) and angiotensin II function in the rat adrenal zona glomerulosa cell.

1994 ◽  
Vol 141 (2) ◽  
pp. R5-R9 ◽  
Author(s):  
G. P. Vinson ◽  
M. M. Ho. ◽  
J.R. Puddefoot ◽  
R. Teja ◽  
S. Barker
Keyword(s):  
Monoclonal Antibody ◽  
Plasma Membrane ◽  
Angiotensin Ii ◽  
Zona Glomerulosa ◽  
Type I ◽  
Specific Monoclonal Antibody ◽  
Angiotensin Ii Receptor ◽  
Cellular Localisation ◽  
Glomerulosa Cells

ABSTRACT Little is known about the cellular localisation of the angiotensin II (AII) type 1 receptor (ATI) in the rat adrenal glomerulosa cell, but some studies have suggested that receptor internalisation and recycling may occur. Using a specific monoclonal antibody (6313/G2) to the first extracellular domain, we show here that most of the receptor is internalised in the unstimulated cell. When viable glomerulosa cells are incubated with 6313/G2, the receptor is transiently concentrated on the cell surface, and aldosterone output is stimulated. This stimulated output is enhanced by neither threshold nor maximal stimulatory concentrations of All amide, although the antibody does not inhibit All binding to the receptor. Conversely, the stimulatory actions of the antibody and those of ACTH are additive. The data suggest that recycling to the plasma membrane is constitutive, or regulated by unknown factors. Retention of the ATI receptor in the membrane is alone enough to allow sufficient G protein interaction to generate maximal stimulatory events.

Inhibition of aldosterone release by hypoxia in vitro: interaction with carbon monoxide

1994 ◽  
Vol 76 (2) ◽  
pp. 689-693 ◽  
Author(s):  
H. Raff ◽  
B. Jankowski
Keyword(s):  
Carbon Monoxide ◽  
Angiotensin Ii ◽  
Zona Glomerulosa ◽  
Michaelis Constant ◽  
Aldosterone Synthase ◽  
Aldosterone Production ◽  
Glomerulosa Cells ◽  
In Vitro Interaction ◽  
Zona Glomerulosa Cells

We have demonstrated that the aldosteronogenic pathway of the zona glomerulosa is unusually sensitive to modest changes in PO2 (Michaelis constant for O2 approximately 95 Torr). The current study evaluated the interaction of CO (the classic ligand for P-450 enzymes) and the decreases in O2 on aldosteronogenesis in vitro. Bovine adrenocortical zona glomerulosa cells were incubated for 2 h and stimulated with either adenosine 3′,5′-cyclic monophosphate (cAMP) or angiotensin II. Ten and 20% CO led to significant decreases in cAMP- and angiotensin II-stimulated aldosteronogenesis. The combination of 20% CO and moderate decreases in PO2 (from approximately 140 to approximately 100 Torr) led to an interactive decrease in aldosterone production. The conversion of corticosterone to aldosterone catalyzed by aldosterone synthase, which is the site of O2 sensitivity, was not significantly inhibited by CO. We conclude that the aldosterone pathway is not exceptionally sensitive to CO compared with other steroidogenic pathways. This observation suggests that the unique O2-sensitive properties of the aldosterone pathway located primarily within aldosterone synthase may not reside in its CO binding site (i.e., heme).

An ultrastructural stereologic study of the effects of angiotensin II on the zona glomerulosa of rat adrenal cortex

1980 ◽  
Vol 95 (4) ◽  
pp. 523-527 ◽  
Author(s):  
Giuseppina Mazzocchi ◽  
Piera Rebuffat ◽  
Anna S. Belloni ◽  
Claudia Robba ◽  
Gastone G. Nussdorfer
Keyword(s):  
Angiotensin Ii ◽  
Smooth Endoplasmic Reticulum ◽  
Zona Glomerulosa ◽  
Significant Rise ◽  
Immunological Methods ◽  
Short Term ◽  
Plasma Aldosterone Concentration ◽  
Noticeable Increase ◽  
Glomerulosa Cells ◽  
Zona Glomerulosa Cells

Abstract. The effects of angiotensin II on the rat zona glomerulosa were investigated by morphometric and radio-immunological methods. Short-term (l h) angiotensin-administration induced lipid depletion in zona glomerulosa cells and a significant rise in the plasma aldosterone concentration. Chronic angiotensin-treatment provoked a noticeable increase in the volume of the zona glomerulosa and its cells, which was mainly due to the hypertrophy of smooth endoplasmic reticulum and mitochondrial compartment. In chronically treated animals the output of aldosterone in response to a short-term stimulation with angiotensin II displayed a significant increase. These findings are interpreted as indicating that angiotensin II is involved in the stimulation of the growth and steroidogenic capacity of the rat zona glomerulosa.

Detection of angiotensin II binding to single adrenal zona glomerulosa cells by confocal Raman microspectroscopy

1999 ◽  
Author(s):  
Michael J. McCoy ◽  
Timothy J. Habermann ◽  
Craig J. Hanke ◽  
Fran Adar ◽  
William B. Campbell ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Zona Glomerulosa ◽  
Raman Microspectroscopy ◽  
Confocal Raman Microspectroscopy ◽  
Glomerulosa Cells ◽  
Confocal Raman ◽  
Zona Glomerulosa Cells

Long-term effects of ACTH combined with angiotensin II on steroidogenesis and adrenal zona glomerulosa morphology in the rat

1987 ◽  
Vol 114 (1) ◽  
pp. 47-54 ◽  
Author(s):  
Anne M. Riondel ◽  
Piera Rebuffat ◽  
Giuseppina Mazzochi ◽  
Gastone G. Nussdorfer ◽  
Rolf C. Gaillard ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Morphological Changes ◽  
Zona Glomerulosa ◽  
Zona Fasciculata ◽  
Homogeneous Population ◽  
Long Term Treatment ◽  
Acth Treatment ◽  
Glomerulosa Cells ◽  
Zona Glomerulosa Cells

Abstract. To test the hypothesis that the trophic action of angiotensin II on the adrenal zona glomerulosa may allow a sustained stimulation of aldosterone by ACTH by preventing the morphological changes of the zona glomerulosa cells into zona fasciculata-like elements we investigated the effects in rats of a 6-day treatment with ACTH (100 μg/kg/day) alone or combined with angiotensin II (300 ng/kg/day) on corticosterone and aldosterone production and adrenal morphology. The responsiveness of both steroids to an acute ACTH dose was also studied on the last day of long-term treatment. Morphologic data showed that prolonged ACTH treatment stimulated the growth of zona glomerulosa cells, though it transformed the tubulo-lamellar cristae of mitochondria into a homogeneous population of vesicles. Angiotensin II furthered the trophic effects of ACTH but prevented the mitochondrial transformation. Despite its ability to conserve the well differentiated aspect of the zona glomerulosa cells, the administration of angiotensin II was unable to prevent the fall in the secretion of aldosterone caused by chronic ACTH treatment and its subsequent unresponsiveness to ACTH stimulation.

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