Open AccessRenal Hydrogen Peroxide Production Prevents Salt‐Sensitive Hypertension
Author(s) -
Cuevas Santiago,
Asico Laureano D.,
Jose Pedro A.,
Konkalmatt Prasad
Publication year - 2020
Publication title -
journal of the american heart association
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.494
H-Index - 85
ISSN - 2047-9980
DOI - 10.1161/jaha.119.013818
Subject(s) - hydrogen peroxide , salt (chemistry) , chemistry , production (economics) , medicine , endocrinology , biochemistry , organic chemistry , economics , macroeconomics
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 H 2 O 2 were higher in renal proximal tubule cells ( RPTC s) from BALB /c than C57Bl/6J mice. High salt diet increased H 2 O 2 production in kidneys from BALB /c but C57Bl/6J mice. High sodium concentration (170 mmol/L) in the incubation medium increased H 2 O 2 levels in BALB /c‐ RPTC s but not in C57Bl/6J‐ RPTC s. H 2 O 2 (10 μmol/L) treatment decreased sodium transport in RPTC s 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 H 2 O 2 production negatively regulates RPTC sodium transport and determines the state of salt sensitivity in 2 strains of mice. High concentrations of antioxidants could prevent H 2 O 2 production in renal proximal tubules, which would result in sodium retention and increased blood pressure.