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Glomerular Expression Of Endothelial Nitric Oxide Synthase In Deoxycorticosterone Acetate‐ Salt‐Treated Rats
Author(s) -
Tsuchiya Ken,
Naruse Mitsuhide,
Nihei Hiroshi
Publication year - 2000
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1046/j.1440-1681.2000.03348.x
Subject(s) - enos , endocrinology , medicine , nitric oxide synthase , glomerulus , messenger rna , nitric oxide synthase type iii , nitric oxide , chemistry , immunohistochemistry , endothelial nos , endothelial nitric oxide synthase , staining , kidney , biology , biochemistry , pathology , gene
SUMMARY 1. In the present study, we investigated the relationship between chronic volume loading and glomerular endothelial nitric oxide synthase (eNOS) expression. Immunohistochemical expression of eNOS in glomeruli was semiquantified by graded scores of staining intensity. Each glomerulus was isolated by microdissection and mRNA expression was detected by reverse transcription–polymerase chain reaction (RT‐PCR) in desoxycorticosterone acetate (DOCA)‐salt‐treated rats. 2. Glomerular expansion and dilatation of tubules were the main histological findings and glomerular and vascular injury scores were significantly higher in the DOCA‐salt‐treated group than in the control group. Endothelial NOS staining in glomeruli in DOCA‐salt‐treated animals was 81.4% lower than in control animals. Endothelial NOS mRNA was also detected at a very low rate in the kidney of treated rats compared with control rats (22/80 vs 74/80 glomeruli, respectively). 3. These results suggest that eNOS protein and mRNA expression in glomeruli was reduced by DOCA‐salt loading. Chronic volume loading may damage the glomerulus and this may be mediated, at least in part, by disruption of eNOS.