Cardiovascular effects of chronically increasing angiotensin II type 2 receptor expression in the nucleus of the solitary tract (874.2)

Angiotensin II (AH) is a potent vasoconstrictor and mitogenic factor. AH receptors include type 1 (ATI) and type 2 (AT2) receptors. Recent studies demonstrated that both ATI and AT2 receptors expressed in human myocardium. Circulating and local tissue level of AH was increased in severe congestive heart failure (CHF). However, the expression of ATI and AT2 in cardiac tissue with CHF remains controversial. Therefore, the present study was designed to investigate the protein expression of ATI and AT2 receptors in normal human myocardium and in human cardiac tissue with mild and severe CHF.Human atrial tissues from normal subjects and CHF patients with ischemic cardiomyopathy and dilated cardiomyopathy were obtained from open-heart surgery and cardiac transplantation. ATI and AT2 receptor expression was investigated by immunohistochemical staining (IHCS). The results of IHCS was evaluated by IHCS staining density scores (0, no staining; 1, minimal staining; 2, mild staining; 3, moderate staining; and 4, strong staining).

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An Intronic Enhancer Element Regulates Angiotensin II Type 2 Receptor Expression during Satellite Cell Differentiation, and Its Activity Is Suppressed in Congestive Heart Failure

Journal of Biological Chemistry ◽

10.1074/jbc.m116.752501 ◽

2016 ◽

Vol 291 (49) ◽

pp. 25578-25590 ◽

Cited By ~ 7

Author(s):

Tadashi Yoshida ◽

Patrice Delafontaine

Keyword(s):

Heart Failure ◽

Congestive Heart Failure ◽

Cell Differentiation ◽

Angiotensin Ii ◽

Satellite Cell ◽

Receptor Expression ◽

Enhancer Element ◽

Intronic Enhancer

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Upregulation of angiotensin II type 2 receptor expression in estrogen-induced pituitary hyperplasia

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.00477.2003 ◽

2004 ◽

Vol 286 (5) ◽

pp. E786-E794 ◽

Cited By ~ 10

Author(s):

Cecilia Suarez ◽

Graciela Díaz-Torga ◽

Arturo González-Iglesias ◽

Carolina Cristina ◽

Damasia Becu-Villalobos

Keyword(s):

Angiotensin Ii ◽

Receptor Expression ◽

Receptor Subtype ◽

At2 Receptor ◽

Ang Ii ◽

Pituitary Hyperplasia ◽

Releasing Effect ◽

At2 Receptors

Recent evidence shows that reexpression and upregulation of angiotensin II (ANG II) type 2 (AT2) receptor in adult tissues occur during pathological conditions such as tissue hyperplasia, inflammation, and remodeling. In particular, expression of functional AT2 receptors in the pituitary and their physiological significance and regulation have not been described. In this study, we demonstrate that chronic in vivo estrogen treatment, which induces pituitary hyperplasia, enhances local AT2 expression (measured by Western blot and RT-PCR) concomitantly with downregulation of ANG II type 1 (AT1) receptors. In vivo progesterone treatment of estrogen-induced pituitary hyperplasia did not modify either the ANG II receptor subtype expression pattern or octapeptide-induced and AT1-mediated calcium signaling. Nevertheless, an unexpected potentiation of the ANG II prolactin-releasing effect was observed in this group, and this response was sensitive to both AT1 and AT2 receptor antagonists. These data are the first to document that ANG II can act at the pituitary level through the AT2 receptor subtype and that estrogens display a differential regulation of AT1 and AT2 receptors at this level.

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Abstract 313: Interferon Regulatory Factor 1 Plays an Important Role in Inhibition of Vascular Remodeling Through Angiotensin II Type 2 Receptor

Hypertension ◽

10.1161/hyp.64.suppl_1.313 ◽

2014 ◽

Vol 64 (suppl_1) ◽

Author(s):

Hirotomo Nakaoka ◽

Masaki Mogi ◽

Jun Suzuki ◽

Harumi Kan-no ◽

Kana Tsukuda ◽

...

Keyword(s):

Oxidative Stress ◽

Angiotensin Ii ◽

Vascular Remodeling ◽

Treated Group ◽

Interferon Regulatory Factor ◽

Receptor Expression ◽

Neointima Formation ◽

Regulatory Factor ◽

Vehicle Treated Group

Objective: Transcriptional control of angiotensin II type 2 (AT 2 ) receptor expression is not well known and we previously reported that interferon regulatory factor (IRF)-1 plays physiological roles in “growth”-regulated AT 2 receptor expression in fibroblast. We studied whether IRF-1 is involved in the attenuation of vascular remodeling in association with AT 2 receptor up-regulation. Methods: Inflammatory vascular injury was induced by polyethylene-cuff placement around the mouse femoral artery in male wild-type mice (WT: C57BL/6J strain), IRF-1 knockout mice (IRF-1KO) and AT 2 receptor-null mice (AT 2 KO) at 10 weeks of age. After cuff placement, each mice were treated with an intraperitoneal injection of compound 21 (C21), AT 2 receptor agonist, at the dose of 10 μg/kg/day or saline. Formalin-fixed, paraffin-embedded sections were prepared using femoral arteries 14 days after cuff placement and subjected to Elastica van Gieson staining for the evaluation of neointima formation. Superoxide anion production and mRNA expressions 7 days after cuff placement were evaluated by dihydroethidium staining and real-time quantitative RT-PCR respectively. Results: Neointima areas in the injured artery induced by cuff placement were significantly increased in vehicle-treated group of IRF-1KO and AT 2 KO compared with those in WT. Moreover, we observed that treatment with C21 attenuated neointima formation 76% in WT, but 45% in IRF-1KO. Oxidative stress was more enhanced in vehicle-treated group of IRF-1KO compared with WT. Treatment with C21 markedly inhibited oxidative stress in WT, but not in IRF-1KO. AT 2 receptor mRNA expression was significantly decreased in IRF-1KO compared with that in WT; however, IRF-1 mRNA expression did not differ between AT 2 KO and WT. Conclusion: These results indicate that IRF-1 up-regulates AT 2 receptor expression and thereby plays an important role in the inhibition of vascular remodeling, supporting the notion that IRF-1 is one of the key transcriptional factor for AT 2 receptor expression and that targeting the immune system is pivotal in the treatment of vascular diseases.

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Angiotensin II type 2 receptor mediated angiotensin II and high glucose induced decrease in renal prorenin/renin receptor expression

Molecular and Cellular Endocrinology ◽

10.1016/j.mce.2009.10.008 ◽

2010 ◽

Vol 315 (1-2) ◽

pp. 188-194 ◽

Cited By ~ 14

Author(s):

Ming He ◽

Lin Zhang ◽

Ying Shao ◽

Hong Xue ◽

Li Zhou ◽

...

Keyword(s):

Angiotensin Ii ◽

High Glucose ◽

Receptor Expression

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Angiotensin II type 1 receptor expression is increased via 12-lipoxygenase in high glucose-stimulated glomerular cells and type 2 diabetic glomeruli

Nephrology Dialysis Transplantation ◽

10.1093/ndt/gfn703 ◽

2008 ◽

Vol 24 (6) ◽

pp. 1744-1752 ◽

Cited By ~ 24

Author(s):

Z.-G. Xu ◽

L.-N. Miao ◽

Y.-C. Cui ◽

Y. Jia ◽

H. Yuan ◽

...

Keyword(s):

Angiotensin Ii ◽

High Glucose ◽

Receptor Expression ◽

12 Lipoxygenase ◽

Type 2 Diabetic

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Angiotensin II type 2 receptor expression in ventricular myocytes does not modify hypertrophic growth under chronic pressure overload

Journal of Cardiac Failure ◽

10.1016/j.cardfail.2004.06.065 ◽

2004 ◽

Vol 10 (4) ◽

pp. S36

Author(s):

Adam J.T. Schuldt ◽

Robert L. Price ◽

Fenfen Liu ◽

Katashi Okoshi ◽

Kalon K.L. Ho ◽

...

Keyword(s):

Angiotensin Ii ◽

Ventricular Myocytes ◽

Pressure Overload ◽

Receptor Expression ◽

Hypertrophic Growth

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Regulation of angiotensin II type 2 receptor gene expression in the adrenal medulla by acute and repeated immobilization stress

Journal of Endocrinology ◽

10.1530/joe-12-0181 ◽

2012 ◽

Vol 215 (2) ◽

pp. 291-301 ◽

Cited By ~ 8

Author(s):

Regina Nostramo ◽

Andrej Tillinger ◽

Juan M Saavedra ◽

Ashok Kumar ◽

Varunkumar Pandey ◽

...

Keyword(s):

Gene Expression ◽

Angiotensin Ii ◽

Receptor Gene ◽

Receptor Expression ◽

Mrna Levels ◽

Ang Ii ◽

Catecholamine Biosynthesis ◽

Receptor Mrna ◽

Receptor Gene Expression

While the renin–angiotensin system is important for adrenomedullary responses to stress, the involvement of specific angiotensin II (Ang II) receptor subtypes is unclear. We examined gene expression changes of angiotensin II type 1A (AT1A) and type 2 (AT2) receptors in rat adrenal medulla in response to immobilization stress (IMO). AT2 receptor mRNA levels decreased immediately after a single 2-h IMO. Repeated IMO also decreased AT2 receptor mRNA levels, but the decline was more transient. AT1A receptor mRNA levels were unaltered with either single or repeated IMO, although binding was increased following repeated IMO. These effects of stress on Ang II receptor expression may alter catecholamine biosynthesis, as tyrosine hydroxylase and dopamine β-hydroxylase mRNA levels in PC12 cells are decreased with Ang II treatment in the presence of ZD7155 (AT1 receptor antagonist) or with CGP42112 (AT2 receptor agonist) treatment. Involvement of stress-triggered activation of the hypothalamic–pituitary–adrenocortical or sympathoadrenal axis in AT2 receptor downregulation was examined. Cultured cells treated with the synthetic glucocorticoid dexamethasone displayed a transcriptionally mediated decrease in AT2 receptor mRNA levels. However, glucocorticoids are not required for the immediate stress-triggered decrease in AT2 receptor gene expression, as demonstrated in corticotropin-releasing hormone knockout (Crh KO) mice and hypophysectomized rats, although they can regulate basal gene expression. cAMP and pituitary adenylate cyclase-activating polypeptide also reduced AT2 receptor gene expression and may mediate this response. Overall, the effects of stress on adrenomedullary AT1A and AT2 receptor expression may contribute to allostatic changes, such as regulation of catecholamine biosynthesis.

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