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Lower oxidative stress is associated with angiotensin II and salt‐induced acute cardiorenal failure in BalbC mice but not C57Black6 (860.10)
Author(s) -
Jonsson Sofia,
Becriovic Agic Mediha,
Tveitaras Maria,
Skogstrand Trude,
Karlsen Tine,
Liden Åsa,
Leh Sabine,
Iversen Bjarne,
Reed Rolf,
Hultström Michael
Publication year - 2014
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.28.1_supplement.860.10
Subject(s) - oxidative stress , excretion , cardiorenal syndrome , medicine , angiotensin ii , endocrinology , tbars , sodium , heart failure , chemistry , blood pressure , lipid peroxidation , organic chemistry
Combined heart and kidney failure has a high mortality rate and no specific treatment. The aim of the present investigation was to identify genetic and physiological differences between a susceptible and a protected mouse strain. In preliminary experiments C57Black6 were found to tolerate angiotensin II (1µg/min/kg AngII) and 5% sodium diet for 5 weeks, while 90% of Balb‐C developed edema, hypotension and acute myocardial and tubular necrosis within four days. Experiments with 0.5µg/min/kg AngII, high sodium diet (3%), or a combination were used for urine collection in metabolic cages and microarray gene expression, which identified enrichment of genes involved in oxidative stress. Water and food intake was similar in the strains. AngII reduced sodium and urine excretion slightly, while salt‐diet alone caused increased excretion in both strains. The combination increased sodium excretion and urine volume more in C57Black6 mice (48%, p<0.05). This was associated with higher oxidative stress in C57Black6 measured as TBARS (125% p<0.01). In conclusion, BalbC are susceptible to acute cardiorenal failure after combined AngII and salt treatment while C57Black6 are not. Global gene expression indicates a difference in oxidative stress. Interestingly, increased oxidative stress was associated with more efficient sodium and volume excretion and protection from cardiorenal failure. Grant Funding Source : Supported by Swedish Heart‐Lung Foundation, Åke Wiberg Foundation, Helsevest Research Council