Premium
SOD1‐deficiency causes salt‐sensitivity and aggravates hypertension in hydronephrosis
Author(s) -
Carlström Mattias,
Brown Russell D.,
Sällström Johan,
Larsson Erik,
Zilmer Mihkel,
Zabihi Sheller,
Eriksson Ulf J.,
Persson Erik G.
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.803.11
Subject(s) - sod1 , medicine , endocrinology , oxidative stress , chemistry , blood pressure , hydronephrosis , excretion , urine , urinary system , superoxide dismutase
We investigated the role of oxidative stress for salt‐sensitivity and for hypertension in hydronephrosis (HN). HN was induced in SOD1‐transgenic (SOD1‐tg), SOD1‐deficient (SOD1‐ko) and wild‐type mice. Telemetric blood pressure measurements were performed during normal and high sodium conditions. Excretion of F2‐IsoP and histology were investigated and the effects of Tempol on blood pressure and TGF were studied. HN wild‐type mice developed salt‐sensitive hypertension (114±1 to 120±2 mmHg) which was augmented in SOD1‐ko mice (125±3 to 135±4 mmHg), but abolished in SOD1‐tr mice (109±3 to 108±3 mmHg). SOD1‐ko controls displayed salt‐sensitive blood pressure (108±1 to 115±2 mmHg), which was not found in wild‐type or SOD1‐tg mice. HN wild‐type and SOD1‐ko mice exhibited increased urine flows, increased urinary excretion of F2‐IsoP, and impaired urine concentration ability. An increased excretion of F2‐IsoP was also found in SOD1‐ko controls. The renal histopathological changes found in HN wild‐types were augmented in SOD1‐ko and diminished in SOD‐tg mice. Tempol attenuated blood pressure and normalized the abnormal TGF in HN. Oxidative stress due to SOD1‐deficiency is associated with salt‐sensitivity and plays an important role for the development of hypertension in HN. Increased superoxide formation can enhance the TGF response and thereby be involved in the development of hypertension.