Role of Type 1 and Type 2 Angiotensin Receptors in Angiotensin II–Induced Cardiomyocyte Hypertrophy

Hypertension ◽  
1996 ◽  
Vol 28 (4) ◽  
pp. 635-640 ◽  
Author(s):  
George W. Booz ◽  
Kenneth M. Baker
Keyword(s):  
Angiotensin Ii ◽  
Angiotensin Receptors ◽  
Cardiomyocyte Hypertrophy

scholarly journals Role of angiotensin II type 2 receptors and kinins in the cardioprotective effect of angiotensin II type 1 receptor antagonists in rats with heart failure

2004 ◽  
Vol 43 (8) ◽  
pp. 1473-1480 ◽  
Author(s):  
Yun-He Liu ◽  
Xiao-Ping Yang ◽  
Edward G. Shesely ◽  
Steadman S. Sankey ◽  
Oscar A. Carretero
Keyword(s):  
Heart Failure ◽  
Angiotensin Ii ◽  
Cardioprotective Effect ◽  
Receptor Antagonists

Angiotensin II type 2 receptor (AT2R) in renal and cardiovascular disease

2016 ◽  
Vol 130 (15) ◽  
pp. 1307-1326 ◽  
Author(s):  
Bryna S.M. Chow ◽  
Terri J. Allen
Keyword(s):  
Angiotensin Ii ◽  
Renin Angiotensin System ◽  
Cellular Growth ◽  
Receptor Subtype ◽  
Electrolyte Balance ◽  
Ang Ii ◽  
Biological Responses

Angiotensin II (Ang II) is well-considered to be the principal effector of the renin–angiotensin system (RAS), which binds with strong affinity to the angiotensin II type 1 (AT1R) and type 2 (AT2R) receptor subtype. However, activation of both receptors is likely to stimulate different signalling mechanisms/pathways and produce distinct biological responses. The haemodynamic and non-haemodynamic effects of Ang II, including its ability to regulate blood pressure, maintain water–electrolyte balance and promote vasoconstriction and cellular growth are well-documented to be mediated primarily by the AT1R. However, its biological and functional effects mediated through the AT2R subtype are still poorly understood. Recent studies have emphasized that activation of the AT2R regulates tissue and organ development and provides in certain context a potential counter-regulatory mechanism against AT1R-mediated actions. Thus, this review will focus on providing insights into the biological role of the AT2R, in particular its actions within the renal and cardiovascular system.

scholarly journals Renal effects of angiotensin II in the newborn period: role of type 1 and type 2 receptors

2016 ◽  
Vol 16 (1) ◽  
Author(s):  
Angela E. Vinturache ◽  
Francine G. Smith
Keyword(s):  
Angiotensin Ii ◽  
Newborn Period ◽  
Renal Effects

scholarly journals A Possible Anti-Inflammatory Role of Angiotensin II Type 2 Receptor in Immune-Mediated Glomerulonephritis during Type 1 Receptor Blockade

2006 ◽  
Vol 169 (5) ◽  
pp. 1577-1589 ◽  
Author(s):  
Hirokazu Okada ◽  
Tsutomu Inoue ◽  
Tomohiro Kikuta ◽  
Yusuke Watanabe ◽  
Yoshihiko Kanno ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Receptor Blockade ◽  
Immune Mediated ◽  
Anti Inflammatory

scholarly journals Role of intracellular angiotensin II

2018 ◽  
Vol 314 (4) ◽  
pp. H766-H771 ◽  
Author(s):  
Richard N. Re
Keyword(s):  
Angiotensin Ii ◽  
Protective Factor ◽  
Intracellular Space ◽  
Neuronal Nuclei ◽  
Disease States ◽  
Animal Physiology ◽  
A Cell

It has become clear that the vasoactive peptide angiotensin II, like other so-called intracrines, can act in the intracellular space. Evidence has accumulated indicating that such angiotensin II activity can be upregulated in disease states and cause pathology. Indeed, other intracrines appear to be involved in disease pathogenesis as well. At the same time, nitric oxide, potentially a cell protective factor, has been shown to be upregulated by intracellular angiotensin II. Recently data have been developed indicating that other potentially protective factors are directly upregulated at neuronal nuclei by angiotensin II. This led to the suggestion that intracellular angiotensin II is cell protective and not pathological. Here, the data on both sides of this issue and a possible resolution are discussed. In summary, there is evidence for both protective and pathological actions of intracellular angiotensin, just as there is abundant evidence derived from whole animal physiology to indicate that angiotensin–driven signaling cascades, including angiotensin II type 2 receptor- and Mas receptor-mediated events, can mitigate the effects of the angiotensin II/angiotensin II type 1 receptor axis (25). This mitigation does not negate the physiological and pathological importance of angiotensin II/angiotensin II type 1 receptor action but does expand our understanding of the workings of both intracellular and extracellular angiotensin II.

scholarly journals Thyroid Hormone Increases TGF-β1 in Cardiomyocytes Cultures Independently of Angiotensin II Type 1 and Type 2 Receptors

2010 ◽  
Vol 2010 ◽  
pp. 1-7 ◽  
Author(s):  
Gabriela Placoná Diniz ◽  
Marcela Sorelli Carneiro-Ramos ◽  
Maria Luiza Morais Barreto-Chaves
Keyword(s):  
Angiotensin Ii ◽  
Cardiac Hypertrophy ◽  
Transforming Growth Factor ◽  
Cardiac Fibroblasts ◽  
Angiotensin Ii Receptors ◽  
Cardiomyocyte Hypertrophy ◽  
Tgf Β1

TH-induced cardiac hypertrophyin vivois accompanied by increased cardiac Transforming Growth Factor-β1 (TGF-β1) levels, which is mediated by Angiotensin II type 1 receptors (AT1R) and type 2 receptors (AT2R). However, the possible involvement of this factor in TH-induced cardiac hypertrophy is unknown. In this study we evaluated whether TH is able to modulate TGF-β1 in isolated cardiac, as well as the possible contribution of AT1R and AT2R in this response. The cardiac fibroblasts treated withT3did not show alteration on TGF-β1 expression. However, cardiomyocytes treated withT3presented an increase in TGF-β1 expression, as well as an increase in protein synthesis. The AT1R blockade prevented theT3-induced cardiomyocyte hypertrophy, while the AT2R blockage attenuated this response. TheT3-induced increase on TGF-β1 expression in cardiomyocytes was not changed by the use of AT1R and AT2R blockers. These results indicate that Angiotensin II receptors are not implicated inT3-induced increase on TGF-βexpression and suggest that the trophic effects exerted byT3on cardiomyocytes are not dependent on the higher TGF-β1 levels, since the AT1R and AT2R blockers were able to attenuate theT3-induced cardiomyocyte hypertrophy but were not able to attenuate the increase on TGF-β1 levels promoted byT3.

Role of 12-lipoxygenase in decreasing P-cadherin and increasing angiotensin II type 1 receptor expression according to glomerular size in type 2 diabetic rats

2011 ◽  
Vol 300 (4) ◽  
pp. E708-E716 ◽  
Author(s):  
Qiao-Yan Guo ◽  
Li-Ning Miao ◽  
Bing Li ◽  
Fu-Zhe Ma ◽  
Nian Liu ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Diabetic Rats ◽  
Ang Ii ◽  
Direct Infusion ◽  
Protein Expressions ◽  
12 Lipoxygenase ◽  
Type 2 Diabetic

12-lipoxygenase (12-LO) was implicated in the development of diabetic nephropathy (DN), in which the proteinuria was thought to be associated with a decreased expression of glomerular P-cadherin. Therefore, we investigated the role of 12-LO in the glomerular P-cadherin expression in type 2 diabetic rats according to the glomerular sizes. Rats fed with high-fat diet for 6 wk were treated with low-dose streptozotocin. Once diabetes onset, diabetic rats were treated with 12-LO inhibitor cinnamyl-3,4-dihydroxy-cyanocinnamate (CDC) for 8 wk. Then glomeruli were isolated from diabetic and control rats with a sieving method. RT-PCR, Western blotting, and immunofluorescent staining were used for mRNA and protein expressions of P-cadherin and angiotensin II (Ang II) type 1 receptor (AT1). We found that CDC did not affect the glucose levels but completely attenuated diabetic increases in glomerular volume and proteinuria. Diabetes significantly decreased the P-cadherin mRNA and protein expressions and increased the AT1 mRNA and protein expressions in the glomeruli. These changes were significantly prevented by CDC and recaptured by direct infusion of 12-LO product [12(S)-HETE] to normal rats for 7 days. The decreased P-cadherin expression was similar between large and small glomeruli, but the increased AT1 expression was significantly higher in the large than in the small glomeruli from diabetic and 12(S)-HETE-treated rats. Direct infusion of normal rats with Ang II for 14 days also significantly decreased the glomerular P-cadherin expression. These results suggest that diabetic proteinuria is mediated by the activation of 12-LO pathway that is partially attributed to the decreased glomerular P-cadherin expression.

Role of angiotensin II type-1 and type-2 receptors on vascular smooth muscle cell growth and glucose metabolism in diabetic rats

2007 ◽  
Vol 75 (3) ◽  
pp. 267-277 ◽  
Author(s):  
Masahiko Igarashi ◽  
Akihiko Hirata ◽  
Hisae Nozaki ◽  
Yuko Kadomoto-Antsuki ◽  
Makoto Tominaga
Keyword(s):  
Smooth Muscle ◽  
Angiotensin Ii ◽  
Cell Growth ◽  
Glucose Metabolism ◽  
Smooth Muscle Cell ◽  
Diabetic Rats ◽  
Smooth Muscle Cell Growth

scholarly journals Role of angiotensin II type 1 (AT1) and type 2 (AT2) receptors in airway reactivity and inflammation in an allergic mouse model of asthma

2019 ◽  
Vol 41 (3) ◽  
pp. 428-437 ◽  
Author(s):  
Mehaben Patel ◽  
Mangesh Kurade ◽  
Sahith Rajalingam ◽  
Riya Bhavsar ◽  
S. Jamal Mustafa ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Mouse Model ◽  
Airway Reactivity ◽  
Allergic Mouse ◽  
At2 Receptors
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