scholarly journals Plasma Total Nitric Oxide and Endothelial Constitutive Nitric Oxide Synthase (ecNOS) Inron 4 Gene Polymorphism: A Study in Children with Chronic Kidney Disease

10.5772/21731 ◽  
2011 ◽  
Author(s):  
Manal F. ◽  
Samar Sabry ◽  
Ahmed Badr ◽  
Eman A. ◽  
Soulaf Kamel ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Chronic Kidney Disease ◽  
Nitric Oxide Synthase ◽  
Kidney Disease ◽  
Gene Polymorphism ◽  
Constitutive Nitric Oxide Synthase ◽  
Oxide Synthase

Triiodothyronine attenuates the progression of renal injury in a rat model of chronic kidney disease

2018 ◽  
Vol 96 (6) ◽  
pp. 603-610 ◽  
Author(s):  
Sahar M. El Agaty
Keyword(s):  
Nitric Oxide ◽  
Chronic Kidney Disease ◽  
Nitric Oxide Synthase ◽  
Kidney Disease ◽  
Renal Injury ◽  
Serum Levels ◽  
Female Rats ◽  
Renal Tubules ◽  
Oxide Synthase ◽  
Remnant Kidney

This study was designed to investigate whether and how triiodothyronine (T3) affects renal function in an experimental model of chronic kidney disease. Twenty-four female rats were divided into the following groups: sham-operated control group (n = 8), 5/6 nephrectomized group (Nx, n = 8), and 5/6 nephrectomized group treated with T3 for 2 weeks (T3-Nx, n = 8). T3 administration significantly decreased serum levels of urea, creatinine, tumour necrosis factorα, and interleukin-6 compared with serum levels in the Nx group. The levels of malondialdehyde, transforming growth factor β, fibronectin, and collagen IV, as well as the expression of inducible nitric oxide synthase, nuclear factor κB, poly(ADP-ribose) polymerase, caspase-3, and Bax were all significantly decreased, though not normalized, in the remnant kidney of rats in the T3-Nx group compared with Nx rats. Glutathione, heme oxygenase-1 levels, as well as endothelial nitric oxide synthase expression were increased in the remnant kidney of the T3-Nx group. Histological studies revealed focal necrosis of renal tubules associated with inflammatory cell infiltration and fibrosis in the Nx group. These changes were alleviated in T3-Nx rats. This study showed that T3 administration attenuated the clinical and histological signs of renal injury in 5/6 nephrectomized rats by mitigating renal oxidative stress, inflammation, apoptosis, and fibrosis.

scholarly journals Endothelial Nitric Oxide Synthase Gene Variation Associated With Chronic Kidney Disease After Liver Transplant

2010 ◽  
Vol 85 (9) ◽  
pp. 814-820 ◽  
Author(s):  
Kiran Bambha ◽  
W. Ray Kim ◽  
Charles B. Rosen ◽  
Rachel A. Pedersen ◽  
Cynthia Rys ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Chronic Kidney Disease ◽  
Nitric Oxide Synthase ◽  
Kidney Disease ◽  
Liver Transplant ◽  
Endothelial Nitric Oxide Synthase ◽  
Gene Variation ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

scholarly journals Endothelial cell transfusion ameliorates endothelial dysfunction in 5/6 nephrectomized rats

2013 ◽  
Vol 305 (8) ◽  
pp. H1256-H1264 ◽  
Author(s):  
Maricica Pacurari ◽  
Dongqi Xing ◽  
Rob H. P. Hilgers ◽  
Yuan Yuan Guo ◽  
Zhengqin Yang ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Chronic Kidney Disease ◽  
Endothelial Dysfunction ◽  
Nitric Oxide Synthase ◽  
Kidney Disease ◽  
Endothelial Nitric Oxide Synthase ◽  
Vascular Function ◽  
Vascular Reactivity ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Endothelial dysfunction is prevalent in chronic kidney disease. This study tested the hypothesis that transfusion of rat aortic endothelial cells (ECs) ameliorates endothelial dysfunction in a rat model of chronic kidney disease. Male Sprague-Dawley rats underwent sham surgery or 5/6 nephrectomy (Nx). Five weeks after Nx, EC (1.5 × 106 cells/rat) or vehicle were transfused intravenously. One week later, vascular reactivity of mesenteric artery was assessed on a wire myograph. Sensitivity of endothelium-dependent relaxation to acetylcholine and maximum vasodilation were impaired by Nx and improved by EC transfusion. Using selective pharmacological nitric oxide synthase isoform inhibitors, we demonstrated that the negative effect of Nx on endothelial function and rescue by EC transfusion are, at least in part, endothelial nitric oxide synthase mediated. Plasma asymmetric dimethylarginine was increased by Nx and decreased by EC transfusion, whereas mRNA expression of dimethylarginine dimethylaminohydrolases 1 (DDAH1) was decreased by Nx and restored by EC transfusion. Immunohistochemical staining confirmed that local expression of DDAH1 is decreased by Nx and increased by EC transfusion. In conclusion, EC transfusion attenuates Nx-induced endothelium-dependent vascular dysfunction by regulating DDAH1 expression and enhancing endothelial nitric oxide synthase activity. These results suggest that EC-based therapy could provide a novel therapeutic strategy to improve vascular function in chronic kidney disease.

Lack of association between endothelial constitutive nitric oxide synthase (ecNOS 4 b/a) gene polymorphism and rheumatic heart disease

2009 ◽  
Vol 19 (6) ◽  
pp. 670-674 ◽  
Author(s):  
Mohamed-mofeed Fawaz Morsy ◽  
Nada Abdelmohsen Abdelaziz ◽  
Ahmed Mohamed Boghdady ◽  
Hydi Ahmed ◽  
Essam Mohamed Abul Fadl ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Heart Disease ◽  
Nitric Oxide Synthase ◽  
Gene Polymorphism ◽  
Rheumatic Heart Disease ◽  
Constitutive Nitric Oxide Synthase ◽  
Oxide Synthase ◽  
Rheumatic Heart

Plasma Total Nitric Oxide and Endothelial Constitutive Nitric Oxide Synthase (ecNOS) Gene Polymorphism: A Study in a South Indian Population

2010 ◽  
Vol 49 (1-2) ◽  
pp. 96-103 ◽  
Author(s):  
Priya Gururajan ◽  
Prema Gurumurthy ◽  
Dolice Victor ◽  
G. Srinivasa Nageswara Rao ◽  
R. Sai Babu ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Gene Polymorphism ◽  
Indian Population ◽  
South Indian Population ◽  
South Indian ◽  
Constitutive Nitric Oxide Synthase ◽  
Oxide Synthase

Endothelial nitric oxide synthase gene intron4 VNTR polymorphism in patients with chronic kidney disease

2011 ◽  
Vol 22 (6) ◽  
pp. 487-492 ◽  
Author(s):  
Manal F. Elshamaa ◽  
Samar Sabry ◽  
Ahmed Badr ◽  
Mostafa El-Ahmady ◽  
Eman A. Elghoroury ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Chronic Kidney Disease ◽  
Nitric Oxide Synthase ◽  
Kidney Disease ◽  
Endothelial Nitric Oxide Synthase ◽  
Vntr Polymorphism ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

scholarly journals Association of endothelial constitutive nitric oxide synthase gene polymorphism with acute coronary syndrome in Koreans

Heart ◽  
2004 ◽  
Vol 90 (3) ◽  
pp. 282-285 ◽  
Author(s):  
K-W Park ◽  
K-H You ◽  
S Oh ◽  
I-H Chae ◽  
H-S Kim ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Gene Polymorphism ◽  
Allele Frequencies ◽  
Control Group ◽  
Genotype Group ◽  
Coronary Syndrome ◽  
Constitutive Nitric Oxide Synthase ◽  
Oxide Synthase ◽  
Genotype And Allele Frequencies

Objective: To examine the effects of two polymorphisms of the endothelial constitutive nitric oxide synthase (ecNOS) gene, 4a/4b(A:B) located in intron 4 and Glu298Asp(G:T) located in exon 7, on the development of acute coronary syndromes (ACS).Methods: 164 patients with ACS and 142 control participants were investigated for genotype and conventional risk factors. Genotype was determined by polymerase chain reaction and restriction fragment length polymorphism analysis.Results: Genotype and allele frequencies of the A:B polymorphism in the ACS group (0.15:0.85 for AA+AB:BB, 0.09:0.91 for A:B) differed from those in the control group (0.26:0.74 for AA+AB:BB, 0.15:0.85 for A:B). However, genotype and allele frequencies of the G:T polymorphism in the ACS group (0.22:0.78 for TT+TG:GG, 0.11:0.89 for T:G) were similar to those in the control group (0.17:0.83 for TT+TG:GG, 0.09:0.91 for T:G). Multiple logistic regression analysis showed that the non-BB (AA+AB) and the non-BB+GG genotypes were significant protective factors against ACS (odds ratios 0.49 and 0.34, 95% confidence intervals 0.26 to 0.93 and 0.14 to 0.83, respectively). In addition, linear association analysis showed that the percentage of ACS patients was significantly lower in the genotype group non-BB+GG than in the genotype group BB+non-GG (39.6% v 62.7%, p  =  0.01).Conclusions: The non-BB genotype of the ecNOS 4a/4b gene polymorphism is a protective factor against the development of ACS. The GG genotype of the ecNOS Glu298Asp polymorphism exerts a benefit in addition to the non-BB genotype in the Korean population.

Sign in / Sign up

Export Citation Format

Share Document