scholarly journals Functional role of angiotensin II AT2 receptor in modulation of AT1 receptor-mediated contraction in rat uterine artery: involvement of bradykinin and nitric oxide

2003 ◽  
Vol 140 (5) ◽  
pp. 987-995 ◽  
Author(s):  
Ruth E Hannan ◽  
Elizabeth A Davis ◽  
Robert E Widdop
Keyword(s):  
Nitric Oxide ◽  
Angiotensin Ii ◽  
Functional Role ◽  
Uterine Artery ◽  
At1 Receptor ◽  
At2 Receptor

scholarly journals Angiotensin II Dilates Bovine Adrenal Cortical Arterioles: Role of Endothelial Nitric Oxide

Endocrinology ◽  
2005 ◽  
Vol 146 (8) ◽  
pp. 3319-3324 ◽  
Author(s):  
Kathryn M. Gauthier ◽  
David X. Zhang ◽  
Erik M. Edwards ◽  
Blythe Holmes ◽  
William B. Campbell
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cell ◽  
Angiotensin Ii ◽  
Receptor Antagonist ◽  
Receptor Activation ◽  
At1 Receptor ◽  
Internal Diameter ◽  
No Production ◽  
At2 Receptor ◽  
Angiotensin Type

Abstract Adrenal steroidogenesis is modulated by humoral and neuronal factors and blood flow. Angiotensin II (AII) stimulates adrenal cortical aldosterone and cortisol production and medullary catecholamine release. However, AII regulation of adrenal vascular tone has not been characterized. We examined the effect of AII on diameters of cannulated bovine adrenal cortical arteries. Cortical arteries (average internal diameter = 230 μm) were constricted with U46619 and concentration-diameter responses to AII (10−13 to 10−8 mol/liter) were measured. In endothelium-intact arteries, AII induced dilations at low concentrations (maximum dilation = 25 ± 6% at 10−10 mol/liter) and constrictions at high concentrations (maximum constriction = 25 ± 18% at 10−8 mol/liter). AII constrictions were blocked by the angiotensin type 1 (AT1) receptor antagonist, losartan (10−6 mol/liter). AII dilations were enhanced by losartan (maximal dilation = 48 ± 8%), abolished by endothelial cell removal or N-nitro-l-arginine (L-NA, 3 × 10−5 mol/liter) and inhibited by the angiotensin type 2 (AT2) receptor antagonist, PD123319 (10−6 mol/liter, maximal dilation = 18 ± 4%). In a 4,5-diaminofluorescein diacetate nitric oxide (NO) assay of isolated cortical arteries, AII stimulated NO production, which was abolished by PD123319, L-NA, or endothelial cell removal. Western immunoblot of arterial homogenates and endothelial and zona glomerulosa cell lysates revealed 48-kD and 50-kD bands corresponding to AT1 and AT2 receptors, respectively, in all three and a 140-kD band corresponding to endothelial NO synthase in endothelial cells and arteries. Our results demonstrate that AII stimulates adrenal cortical arterial dilation through endothelial cell AT2 receptor activation and NO release and AT1 receptor-dependent constriction.

scholarly journals Valsartan prevented neointimal hyperplasia and inhibited SRSF1 expression and the TLR4–iNOS–ERK–AT1 receptor pathway in the balloon-injured rat aorta

2021 ◽  
pp. 533-542
Author(s):  
Yonghong Li ◽  
Junjie Guo ◽  
Haichu Yu ◽  
Xin Liu ◽  
Jingwei Zhou ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Angiotensin Ii ◽  
Nitric Oxide Synthase ◽  
Protein Expression ◽  
Neointimal Hyperplasia ◽  
Treated Group ◽  
Rat Aorta ◽  
At1 Receptor ◽  
At2 Receptor ◽  
Oxide Synthase

Valsartan has the potential to attenuate neointimal hyperplasia and to suppress the inflammatory response. This study aimed to evaluate the role of valsartan in neointimal hyperplasia and the toll-like receptor 4 (TLR4)-nitric oxide synthase (NOS) pathway in the balloon-injured rat aorta. Forty-eight Wistar rats were randomly allocated to three groups: sham control (control), balloon-injured group (surgery), and balloon-injured+valsartan-treated group (valsartan). Rats were killed at 14 and 28 days after balloon-injury, and then the aortic tissues were collected for morphometric analysis as well as for measurements of the mRNA or protein expression of angiotensin II, angiotensin II type 1 (AT1) receptor, angiotensin II type 2 (AT2) receptor, TLR4, endothelial nitric oxide synthase (eNOS), inducible NOS (iNOS), serine/arginine-rich splicing factor 1(SRSF1) and extracellular signal regulated kinase (ERK). Valsartan at a dose of 20 mg/kg/day markedly decreased neointimal hyperplasia in the aorta of balloon-injured rats, and significantly reduced the mRNA or protein expression of TLR4, AT1 receptor, SRSF1 and phosphorylated-ERK (p-ERK) as well as the aortic levels of iNOS (all p<0.05). Moreover, valsartan increased the eNOS level and AT2 receptor mRNA and protein expression levels (all p<0.05). Valsartan prevented neointimal hyperplasia and inhibited SRSF1 expression and the TLR4-iNOS-ERK-AT1 receptor pathway in the balloon-injured rat aorta.

scholarly journals Mesangial Cells Cultured from Pregnant Rats Display Reduced Reactivity to Angiotensin II: the Role of Relaxin, Nitric Oxide and AT2 Receptor

2012 ◽  
Vol 30 (6) ◽  
pp. 1456-1464 ◽  
Author(s):  
Lucimeire N. Carvalho ◽  
Priscila C. Cristovam ◽  
Clévia S. Passos ◽  
Mirian A. Boim
Keyword(s):  
Nitric Oxide ◽  
Angiotensin Ii ◽  
Mesangial Cells ◽  
At2 Receptor ◽  
Pregnant Rats ◽  
Cells Cultured

scholarly journals Emerging Role of Angiotensin AT2 Receptor in Anti-Inflammation: An Update

2020 ◽  
Vol 26 (4) ◽  
pp. 492-500 ◽  
Author(s):  
Sanket N. Patel ◽  
Naureen Fatima ◽  
Riyasat Ali ◽  
Tahir Hussain
Keyword(s):  
Nitric Oxide ◽  
Angiotensin Ii ◽  
Cell Survival ◽  
Immune Cells ◽  
Therapeutic Target ◽  
At2 Receptor ◽  
Pathological Conditions ◽  
Promote Cell Survival ◽  
Anti Inflammation

The hyperactive RAS and inflammation are closely associated. The angiotensin-II/AT1R axis of the RAS has been explored extensively for its role in inflammation and a plethora of pathological conditions. Understanding the role of AT2R in inflammation is an emerging area of research. The AT2R is expressed on a variety of immune and non-immune cells, which upon activation triggers the release of a host of cytokines and has multiple effects that coalesce to anti-inflammation and prevents maladaptive repair. The anti-inflammatory outcomes of AT2R activation are linked to its well-established signaling pathways involving formation of nitric oxide and activation of phosphatases. Collectively, these effects promote cell survival and tissue function. The consideration of AT2R as a therapeutic target requires further investigations.

ACE2/Angiotensin-(1-7)/Mas Receptor Axis in Human Cancer: Potential Role for Pediatric Tumors

2020 ◽  
Vol 21 (9) ◽  
pp. 892-901 ◽  
Author(s):  
Ana Luiza Ataide Carneiro de Paula Gonzaga ◽  
Vitória Andrade Palmeira ◽  
Thomas Felipe Silva Ribeiro ◽  
Larissa Braga Costa ◽  
Karla Emília de Sá Rodrigues ◽  
...  
Keyword(s):  
Clinical Trials ◽  
Angiotensin Ii ◽  
Pediatric Cancer ◽  
Pediatric Patients ◽  
Human Cancer ◽  
Experimental Studies ◽  
At1 Receptor ◽  
Pediatric Tumors ◽  
Mas Receptor

Background: Pediatric tumors remain the highest cause of death in developed countries. Research on novel therapeutic strategies with lesser side effects is of utmost importance. In this scenario, the role of Renin-Angiotensin System (RAS) axes, the classical one formed by angiotensinconverting enzyme (ACE), Angiotensin II and AT1 receptor and the alternative axis composed by ACE2, Angiotensin-(1-7) and Mas receptor, have been investigated in cancer. Objective: This review aimed to summarize the pathophysiological role of RAS in cancer, evidence for anti-tumor effects of ACE2/Angiotensin-(1-7)/Mas receptor axis and future therapeutic perspectives for pediatric cancer. Methods: Pubmed, Scopus and Scielo were searched in regard to RAS molecules in human cancer and pediatric patients. The search terms were “RAS”, “ACE”, “Angiotensin-(1-7)”, “ACE2”, “Angiotensin II”, “AT1 receptor”, “Mas receptor”, “Pediatric”, “Cancer”. Results: Experimental studies have shown that Angiotensin-(1-7) inhibits the growth of tumor cells and reduces local inflammation and angiogenesis in several types of cancer. Clinical trials with Angiotensin-( 1-7) or TXA127, a pharmaceutical grade formulation of the naturally occurring peptide, have reported promising findings, but not enough to recommend medical use in human cancer. In regard to pediatric cancer, only three articles that marginally investigated RAS components were found and none of them evaluated molecules of the alternative RAS axis. Conclusion: Despite the potential applicability of Angiotensin-(1-7) in pediatric tumors, the role of this molecule was never tested. Further clinical trials are necessary, also including pediatric patients, to confirm safety and efficiency and to define therapeutic targets.

Role of Nitric Oxide in Short-term and Prolonged Effects of Angiotensin II on Renal Hemodynamics

Hypertension ◽  
1996 ◽  
Vol 27 (5) ◽  
pp. 1173-1179 ◽  
Author(s):  
Xiaolin Deng ◽  
William J. Welch ◽  
Christopher S. Wilcox
Keyword(s):  
Nitric Oxide ◽  
Angiotensin Ii ◽  
Renal Hemodynamics ◽  
Short Term
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