Nitric oxide, oxidative stress, and progression of chronic renal failure

2004 ◽  
Vol 24 (4) ◽  
pp. 354-365 ◽  
Author(s):  
Paul S Modlinger ◽  
Christopher S Wilcox ◽  
Shakil Aslam
2000 ◽  
Vol 279 (6) ◽  
pp. H2786-H2796 ◽  
Author(s):  
Shaohua Ye ◽  
Pantea Mozayeni ◽  
Michael Gamburd ◽  
Huiqin Zhong ◽  
Vito M. Campese

Increased sympathetic nervous system (SNS) activity plays a role in the genesis of hypertension in rats with chronic renal failure (CRF). The rise in central SNS activity is mitigated by increased local expression of neuronal nitric oxide synthase (NOS) mRNA and NO2/NO3 production. Because interleukin (IL)-1β may activate nitric oxide in the brain, we have tested the hypothesis that IL-1β may modulate the activity of the SNS via regulation of the local expression of neuronal NOS (nNOS) in the brain of CRF and control rats. To this end, we first found that administration of IL-1β in the lateral ventricle of control and CRF rats decreased blood pressure and norepinephrine (NE) secretion from the posterior hypothalamus (PH) and increased NOS mRNA expression. Second, we observed that an acute or chronic injection of an IL-1β-specific antibody in the lateral ventricle raised blood pressure and NE secretion from the PH and decreased NOS mRNA abundance in the PH of control and CRF rats. Finally, we measured the IL-1β mRNA abundance in the PH, locus coeruleus, and paraventricular nuclei of CRF and control rats by RT-PCR and found it to be greater in CRF rats than in control rats. In conclusion, these studies have shown that IL-1β modulates the activity of the SNS in the central nervous system and that this modulation is mediated by increased local expression of nNOS mRNA.


RSC Advances ◽  
2015 ◽  
Vol 5 (25) ◽  
pp. 19337-19344 ◽  
Author(s):  
Jeganathan Manivannan ◽  
Janakiraman Shanthakumar ◽  
Thangarasu Silambarasan ◽  
Elumalai Balamurugan ◽  
Boobalan Raja

Prevention of hypertension, cardiac remodeling and oxidative stress in chronic renal failure (CRF) rats by diosgenin.


ASAIO Journal ◽  
2006 ◽  
Vol 52 (2) ◽  
pp. 75A ◽  
Author(s):  
J Simoni ◽  
G Simoni ◽  
J F Moeller ◽  
A Khanna ◽  
W T Bohannon ◽  
...  

Nutrients ◽  
2017 ◽  
Vol 9 (8) ◽  
pp. 895 ◽  
Author(s):  
Michela Zanetti ◽  
Gianluca Gortan Cappellari ◽  
Davide Barbetta ◽  
Annamaria Semolic ◽  
Rocco Barazzoni

2011 ◽  
Vol 29 (3) ◽  
pp. 249-254 ◽  
Author(s):  
Şerafettin Demirci ◽  
Mehmet Ramazan Şekeroğlu ◽  
Tevfik Noyan ◽  
Ruşen Köçeroğlu ◽  
Yasemin Usul Soyoral ◽  
...  

2016 ◽  
Vol 38 (5) ◽  
pp. 1703-1713 ◽  
Author(s):  
Abderrahim Nemmar ◽  
Turan Karaca ◽  
Sumaya Beegam ◽  
Priya Yuvaraju ◽  
Javed Yasin ◽  
...  

Background/Aims: Epidemiological evidence indicates that patients with chronic kidney diseases have increased susceptibility to adverse outcomes related to long-term exposure to particulate air pollution. However, mechanisms underlying these effects are not fully understood. Methods: Presently, we assessed the effect of prolonged exposure to diesel exhaust particles (DEP) on chronic renal failure induced by adenine (0.25% w/w in feed for 4 weeks), which is known to involve inflammation and oxidative stress. DEP (0.5m/kg) was intratracheally (i.t.) instilled every 4th day for 4 weeks (7 i.t. instillation). Four days following the last exposure to either DEP or saline (control), various renal endpoints were measured. Results: While body weight was decreased, kidney weight increased in DEP+adenine versus saline+adenine or DEP. Water intake, urine volume, relative kidney weight were significantly increased in adenine+DEP versus DEP and adenine+saline versus saline. Plasma creatinine and urea increased and creatinine clearance decreased in adenine+DEP versus DEP and adenine+saline versus saline. Tumor necrosis factor α, lipid peroxidation and reactive oxygen species were significantly increased in adenine+DEP compared with either DEP or adenine+saline. The antioxidant calase was significantly decreased in adenine+DEP compared with either adenine+saline or DEP. Notably, renal DNA damage was significantly potentiated in adenine+DEP compared with either adenine+saline or DEP. Similarly, systolic blood pressure was increased in adenine+DEP versus adenine+saline or DEP, and in DEP versus saline. Histological evaluation revealed more collagen deposition, higher number of necrotic cell counts and dilated tubules, cast formation and collapsing glomeruli in adenine+DEP versus adenine+saline or DEP. Conclusion: Prolonged pulmonary exposure to diesel exhaust particles worsen renal oxidative stress, inflammation and DNA damage in mice with adenine-induced chronic renal failure. Our data provide biological plausibility that air pollution aggravates chronic renal failure.


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