Alteration of Nitric Oxide Synthase and Guanylyl Cyclase Activity in Rats with Ischemia/Reperfusion Renal Injury.
- Author:
Eun Hui BAE
1
;
Soo Wan KIM
Author Information
1. Department of Internal Medicine, Chonnam National University Medical School, Gwangju, Korea. skimw@chonnam.ac.kr
- Publication Type:Original Article
- Keywords:
Nitric oxide synthase;
Ischemic/perfusion injury;
cGMP
- MeSH:
Animals;
Blotting, Western;
Constriction;
Guanosine;
Guanylate Cyclase*;
Humans;
Male;
Neurons;
Nitric Oxide Synthase*;
Nitric Oxide*;
Nitroprusside;
Osmolar Concentration;
Protein Isoforms;
Rats*;
Rats, Sprague-Dawley;
Renal Insufficiency;
Tissue Donors
- From:The Korean Journal of Physiology and Pharmacology
2006;10(6):337-341
- CountryRepublic of Korea
- Language:English
-
Abstract:
The present study was designed to investigate the protein expression of nitric oxide synthase (NOS) and guanylyl cyclase (GC) activity in ischemia/perfusion (I/R) renal injury in rats. Renal I/R injury was experimentally induced by clamping the both renal pedicle for 40 min in Sprague-Dawley male rats. The renal expression of NOS isoforms was determined by Western blot analysis, and the activity of guanylyl cyclase was determined by the amount of guanosine 3', 5'-cyclic monophosphate (cGMP) formed in response to sodium nitroprusside (SNP), NO donor. I/R injury resulted in renal failure associated with decreased urine osmolality. The expression of inducible NOS (iNOS) was increased in I/R injury rats compared with controls, while endothelial NOS (eNOS) and neuronal NOS (nNOS) expression was decreased. The urinary excretion of NO metabolites was decreased in I/R injury rats. The cGMP production provoked by SNP was decreased in the papilla, but not in glomerulus. These results indicate an altered regulation of NOS expression and guanylyl cyclase activity in I/R-induced nephropathy.
