The effect of a nitric oxide donor on endogenous endothelin-1 expression in renal ischemia/reperfusion injury

2004 ◽  
Vol 36 (7) ◽  
pp. 1943-1945 ◽  
Author(s):  
G.-Y. Jeong ◽  
K.-Y. Chung ◽  
W.J. Lee ◽  
Y.S. Kim ◽  
S.H. Sung
Keyword(s):  
Nitric Oxide ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Renal Ischemia ◽  
Nitric Oxide Donor ◽  
Endothelin 1 ◽  
Renal Ischemia Reperfusion Injury

Role of Glyceryl Trinitrate, a Nitric Oxide Donor, in the Renal Ischemia-Reperfusion Injury of Rats

2006 ◽  
Vol 38 (5) ◽  
pp. 431-437 ◽  
Author(s):  
Hasan Fehmi Kucuk ◽  
Levent Kaptanoglu ◽  
Figen Ozalp ◽  
Necmi Kurt ◽  
Sadık Bingul ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Glyceryl Trinitrate ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Renal Ischemia ◽  
Nitric Oxide Donor ◽  
Renal Ischemia Reperfusion Injury

Nitrite, a hypoxia selective nitric oxide donor, limits renal ischemia-reperfusion injury in non-human primates

2006 ◽  
Vol 203 (3) ◽  
pp. S31
Author(s):  
Kiran K. Dhanireddy ◽  
David A. Bruno ◽  
Sruti Shiva ◽  
Frank V. Leopardi ◽  
Xiaojie Zhang ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Renal Ischemia ◽  
Nitric Oxide Donor ◽  
Renal Ischemia Reperfusion Injury

Intrarenal Administration of Molsidomine, a Molecule Releasing Nitric Oxide, Reduces Renal Ischemia-Reperfusion Injury in Rats

2004 ◽  
Vol 4 (10) ◽  
pp. 1605-1613 ◽  
Author(s):  
Ana Rodriguez-Pena ◽  
Francisco J. Garcia-Criado ◽  
Nelida Eleno ◽  
Miguel Arevalo ◽  
Jose M. Lopez-Novoa
Keyword(s):  
Nitric Oxide ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Renal Ischemia ◽  
Renal Ischemia Reperfusion Injury

scholarly journals Inhibition of inducible nitric oxide synthase reduces renal ischemia/reperfusion injury

2002 ◽  
Vol 61 (3) ◽  
pp. 862-871 ◽  
Author(s):  
Prabal K. Chatterjee ◽  
Nimesh S.A. Patel ◽  
Espen O. Kvale ◽  
Salvatore Cuzzocrea ◽  
Paul A.J. Brown ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Reperfusion Injury ◽  
Inducible Nitric Oxide Synthase ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Renal Ischemia ◽  
Renal Ischemia Reperfusion Injury ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

The role of nitric oxide pathway in the renal ischemia–reperfusion injury in rats

2002 ◽  
Vol 10 (4) ◽  
pp. 277-284 ◽  
Author(s):  
Ernani Luı́s Rhoden ◽  
Cláudia Ramos Rhoden ◽  
Márcio Luı́s Lucas ◽  
Luiz Pereira-Lima ◽  
Cláudio Zettler ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Renal Ischemia ◽  
Renal Ischemia Reperfusion Injury ◽  
Nitric Oxide Pathway

scholarly journals Deletion of the Gamma Subunit of ENaC in Endothelial Cells Does Not Protect against Renal Ischemia Reperfusion Injury

2021 ◽  
Vol 22 (20) ◽  
pp. 10914
Author(s):  
Stephanie M. Mutchler ◽  
Mahpara Hasan ◽  
Donald E. Kohan ◽  
Thomas R. Kleyman ◽  
Roderick J. Tan
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Kidney Injury ◽  
Renal Ischemia ◽  
Α Subunit ◽  
Γ Subunit ◽  
Renal Ischemia Reperfusion Injury

Acute kidney injury due to renal ischemia-reperfusion injury (IRI) may lead to chronic or end stage kidney disease. A greater understanding of the cellular mechanisms underlying IRI are required to develop therapeutic options aimed at limiting or reversing damage from IRI. Prior work has shown that deletion of the α subunit of the epithelial Na+ channel (ENaC) in endothelial cells protects from IRI by increasing the availability of nitric oxide. While canonical ENaCs consist of an α, β, and γ subunit, there is evidence of non-canonical ENaC expression in endothelial cells involving the α subunit. We therefore tested whether the deletion of the γ subunit of ENaC also protects mice from IRI to differentiate between these channel configurations. Mice with endothelial-specific deletion of the γ subunit and control littermates were subjected to unilateral renal artery occlusion followed by 48 h of reperfusion. No significant difference was noted in injury between the two groups as assessed by serum creatinine and blood urea nitrogen, levels of specific kidney injury markers, and histological examination. While deletion of the γ subunit did not alter infiltration of immune cells or cytokine message, it was associated with an increase in levels of total and phosphorylated endothelial nitric oxide synthase (eNOS) in the injured kidneys. Our studies demonstrate that even though deletion of the γ subunit of ENaC may allow for greater activation of eNOS, this is not sufficient to prevent IRI, suggesting the protective effects of α subunit deletion may be due, in part, to other mechanisms.

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