title: [Primary study on the effects of high-salt diet on the myocardium and the related mechanisms].
abstract: OBJECTIVE
  The study was to evaluate the effects of high-salt diet on the blood pressure and myocardium in Sprague-Dawley rats and to investigate the related mechanisms.
  
  
  METHODS
  Rat model of high-salt diet was established by receiving standard rat chow with salt concentration of 0.3% and additional salt load via the drinking water (1% sodium chloride solution). Systolic blood pressure was measured by The indirect tail-cuff method in the rats on high-salt and normal-salt diet. The rats were placed in metabolic cages. Food intake and urine volume were recorded. The sodium and chloride in plasma and urine were measured. Transthoracic echocardiographic studies were performed at the eighth week with an echocardiographic system. The pathological variations of the myocardium were observed by the electron microscopy. The p22phox and p47phox mRNA expressions were analyzed by real time RT-PCR. The p22phox and p47phox protein expressions were analyzed by Western blot. The NADPH oxidase activity of myocardium and the serum 8-isoprostane levels were measured.
  
  
  RESULTS
  Left ventricular hypertrophy (all P < 0.05) and the decreased diastolic function of left ventricle without significantly elevated blood pressure [(128 +/- 4) mm Hg versus (125 +/- 3) mm Hg in controls, P > 0.05] were found in the rats on high-salt diet, compared to those in the rats on normal-salt diet. Furthermore, mRNA and protein expressions of the p22phox and p47phox, and the NADPH oxidase activity of myocardium were increased [(0.332 +/- 0.015) micromol x min(-1) x mg(-1) versus (0.142 +/- 0.023) micromol x min(-1) x mg(-1) in controls, P <0.05]. Serum 8-isoprostane levels [(1117 +/- 86) pg/ml versus (327 +/- 80) pg/ml in controls, P < 0.05] were also significantly increased in the rats on high-salt diet.
  
  
  CONCLUSIONS
  High-salt diet might lead to left ventricular hypertrophy and the decreased diastolic function of left ventricle through oxidative stress without significantly elevated blood pressure.
authors: Department of Endocrinology, the Second Affiliated Hospital, Sun Yat-sen University, Guangzhou 510120, China.
authors: Jing-Yi
authors: JY
authors: Li
authors: Shao-Ling
authors: SL
authors: Zhang
authors: Li
authors: L
authors: Yan
authors: Meng
authors: M
authors: Ren
authors: Chuan
authors: C
authors: Wang
authors: Hua
authors: H
authors: Cheng
mesh_terms: D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D015237:Dinoprost / Q000031:analogs & derivatives / Q000097:blood; D017379:Hypertrophy, Left Ventricular / Q000139:chemically induced*; D008297:Male; D019255:NADPH Oxidases / Q000378:metabolism; D018384:Oxidative Stress; D051381:Rats; D017207:Rats, Sprague-Dawley; D017673:Sodium Chloride, Dietary / Q000009:adverse effects*
chemical_list: D017673:Sodium Chloride, Dietary; C075750:8-epi-prostaglandin F2alpha; D015237:Dinoprost; D019255:NADPH Oxidases; C515768:Cyba protein, rat; C060505:neutrophil cytosolic factor 1