| Autor: |
Santiago Cuevas, Laureano D. Asico, Pedro A. Jose, Prasad Konkalmatt |
| Jazyk: |
angličtina |
| Rok vydání: |
2020 |
| Předmět: |
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| Zdroj: |
Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease, Vol 9, Iss 1 (2020) |
| Druh dokumentu: |
article |
| ISSN: |
2047-9980 |
| DOI: |
10.1161/JAHA.119.013818 |
| Popis: |
Background The regulation of sodium excretion is important in the pathogenesis of hypertension and salt sensitivity is predictive of cardiovascular events and mortality. C57Bl/6 and BALB/c mice have different blood pressure sensitivities to salt intake. High salt intake increases blood pressure in some C57Bl/6J mouse strains but not in any BALB/c mouse strain. Methods and Results We determined the cause of the difference in salt sensitivity between C57Bl/6 and BALB/c mice. Basal levels of superoxide and H2O2 were higher in renal proximal tubule cells (RPTCs) from BALB/c than C57Bl/6J mice. High salt diet increased H2O2 production in kidneys from BALB/c but C57Bl/6J mice. High sodium concentration (170 mmol/L) in the incubation medium increased H2O2 levels in BALB/c‐RPTCs but not in C57Bl/6J‐RPTCs. H2O2 (10 μmol/L) treatment decreased sodium transport in RPTCs from BALB/c but not C57Bl/6J mice. Overexpression of catalase in the mouse kidney predisposed BALB/c mice to salt‐sensitive hypertension. Conclusions Our data show that the level of salt‐induced H2O2 production negatively regulates RPTC sodium transport and determines the state of salt sensitivity in 2 strains of mice. High concentrations of antioxidants could prevent H2O2 production in renal proximal tubules, which would result in sodium retention and increased blood pressure. |
| Databáze: |
Directory of Open Access Journals |
| Externí odkaz: |
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