Abstract:
: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.
journal_name
J Am Heart Assocjournal_title
Journal of the American Heart Associationauthors
Cuevas S,Asico LD,Jose PA,Konkalmatt Pdoi
10.1161/JAHA.119.013818subject
Has Abstractpub_date
2020-01-07 00:00:00pages
e013818issue
1issn
2047-9980journal_volume
9pub_type
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