title: N-Acetylcysteine improves renal dysfunction, ameliorates kidney damage and decreases blood pressure in salt-sensitive hypertension.
abstract: BACKGROUND
  Salt-sensitive hypertension in humans and experimental animals causes progressive increases in renal damage and dysfunction. The Dahl salt-sensitive (S) rat closely mimics human salt-sensitive hypertension.
  
  
  OBJECTIVE
  Our goal was to test the hypothesis that enhancing the glutathione system with dietary N-acetylcysteine administration in Dahl S rats on a high sodium intake for 5 weeks will attenuate the increases in arterial pressure, the decreases in renal hemodynamics and the increases in renal damage that normally occur in S rats on high sodium.
  
  
  METHODS
  Forty-four 7- to 8-week-old Dahl S/Rapp strain rats were maintained on a high sodium (8%), high sodium + N-acetylcysteine (4 g/kg per day), or low sodium (0.3%) diet for 5 weeks. Rats had arterial and venous catheters implanted at day 21.
  
  
  RESULTS
  By day 35 in the high-sodium rats, N-acetylcysteine treatment significantly increased the renal reduced-to-oxidized glutathione ratio, glomerular filtration rate, and renal plasma flow, and decreased renal cortical and medullary O2 release, urinary protein excretion, renal tubulointerstitial damage and glomerular necrosis. At this time, mean arterial pressure increased to 183 +/- 1 mmHg, and N-acetylcysteine reduced this arterial pressure to 121 +/- 4 mmHg. By day 35 in S high-sodium rats, N-acetylcysteine had caused a 91% decrease in glomerular necrosis and an 83% decrease in tubulointerstitial damage.
  
  
  CONCLUSIONS
  In Dahl S rats on high sodium intake, arterial pressure increases significantly and renal injury is pronounced. Treatment with N-acetylcysteine enhances the renal glutathione system, improves renal dysfunction and markedly decreases arterial pressure and renal injury in Dahl salt-sensitive hypertension.
authors.affiliation: Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, Mississippi 39216, USA. ntian@physiology.umsmed.edu
authors.forename: Niu
authors.initials: N
authors.lastname: Tian
authors.forename: Rebecca A
authors.initials: RA
authors.lastname: Rose
authors.forename: Sharkeshia
authors.initials: S
authors.lastname: Jordan
authors.forename: Terry M
authors.initials: TM
authors.lastname: Dwyer
authors.forename: Michael D
authors.initials: MD
authors.lastname: Hughson
authors.forename: R Davis
authors.initials: RD
authors.lastname: Manning
mesh_terms: D000111:Acetylcysteine / Q000494:pharmacology*; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D004195:Disease Models, Animal; D016166:Free Radical Scavengers / Q000494:pharmacology*; D005919:Glomerular Filtration Rate / Q000187:drug effects; D005978:Glutathione / Q000032:analysis / Q000187:drug effects*; D006973:Hypertension / Q000188:drug therapy*; D007674:Kidney Diseases / Q000188:drug therapy* / Q000473:pathology; D008297:Male; D018384:Oxidative Stress / Q000187:drug effects / Q000502:physiology; D051381:Rats; D020303:Rats, Inbred Dahl; D017673:Sodium Chloride, Dietary / Q000037:antagonists & inhibitors* / Q000494:pharmacology
chemical_list: D016166:Free Radical Scavengers; D017673:Sodium Chloride, Dietary; D005978:Glutathione; D000111:Acetylcysteine