title: [Up-regulation of intrarenal renin-angiotensin system contributes to renal damage in high-salt induced hypertension rats].
abstract: OBJECTIVE
  To test the hypothesis that in a high-salt induced hypertension in normal rats, whether the changes of intrarenal renin-agiotensin system (RAS) play a critical role in renal damage and could be reflected by urinary angiotensinogen (AGT).
  
  
  METHODS
  In the study, 27 normotensive male Wistar-Kyoto rats were divided into control group [0.3% (mass faction) NaCl in chow, n=9, NS], high-salt diet group [8% (mass faction) NaCl in chow, n=9, HS] and high-salt diet with Losartan group [8% (mass faction) NaCl in chow and 20 mg/(kg×d) Losartan in gavages, n=9, HS+L)], and were fed for six weeks. The blood pressure was monitored and urine samples were collected every 2 weeks. AGTs in plasma, kidney and urine were measured by ELISA kits. The renal cortex expression of mRNA and protein of AGT were measured by Real-time PCR and immunohistochemistry (IHC). The renin activity and ANG II were measured by radioimmunoassay (RIA) kits.
  
  
  RESULTS
  Compared with NS, the systolic blood pressure (SBP) [(156 ± 2) mmHg vs. (133 ± 3) mmHg, P<0.05] increased significantly at the end of the 2nd week, and the urinary protein [(14.07 ± 2.84) mg/24 h vs. (7.62 ± 3.02) mg/24 h, P<0.05] increased significantly at the end of the 6th week in HS. Compared with HS, there was no significant difference in SBP (P>0.05) but the proteinuria [(9.69 ± 2.73) mg/24 h vs. (14.07 ± 2.84) mg/24 h, P<0.01] decreased significantly in HS+L. Compared with NS, there was no significant difference in the plasma renin activity, angiotensinogen and ANG II level in HS (P>0.05), but the renal cortex renin content [(8.72 ± 1.98) ng/(mL × h) vs. (4.37 ± 1.26) ng/(mL × h), P<0.05], AGT formation [(4.02 ± 0.60) ng/mg vs. (2.59 ± 0.42) ng/mg, P<0.01], ANG II level [(313.8 ± 48.76) pmol/L vs. (188.9 ± 46.95) pmol/L, P<0.05] were increased significantly in HS, and the urinary AGT and ANG II excretion rates increased significantly (P<0.05). Compared with HS, the plasma renin activity, angiotensinogen and ANG II level were significantly increased (P<0.05), but the renal cortex renin content, AGT formation, ANG II level significantly decreased (P<0.05), and the urinary AGT and ANG II excretion rates decreased significantly in HS+L (P<0.05). The urinary AGT excretion rates were positively correlated with the AGT level in the renal cortex (P<0.05).
  
  
  CONCLUSIONS
  Up-regulation of intarenal RAS may contribute to renal damage in high-salt induced hypertension rats. Urinary AGT may reflect the status of intrarenal RAS.
authors: Department of Nephrology, Peking University Third Hospital, Beijing 100191, China.
authors: Hai-yan
authors: HY
authors: Wu
authors: Department of Nephrology, Peking University Third Hospital, Beijing 100191, China.
authors: Yao-xian
authors: YX
authors: Liang
authors: Department of Nephrology, Peking University Third Hospital, Beijing 100191, China.
authors: Qiong
authors: Q
authors: Bai
authors: Department of Nephrology, Peking University Third Hospital, Beijing 100191, China.
authors: Zhen
authors: Z
authors: Zhuang
authors: Department of Nephrology, Peking University Third Hospital, Beijing 100191, China.
authors: La-ta
authors: LT
authors: A
authors: Department of Nephrology, Peking University Third Hospital, Beijing 100191, China.
authors: Dan-xia
authors: DX
authors: Zheng
authors: Department of Nephrology, Peking University Third Hospital, Beijing 100191, China.
authors: Yue
authors: Y
authors: Wang
mesh_terms: D000804:Angiotensin II / Q000378:metabolism*; D000808:Angiotensinogen / Q000378:metabolism*; D000818:Animals; D001794:Blood Pressure; D004195:Disease Models, Animal; D006973:Hypertension / Q000139:chemically induced / Q000503:physiopathology*; D007668:Kidney / Q000473:pathology*; D008297:Male; D011507:Proteinuria; D051381:Rats; D011921:Rats, Inbred WKY; D060888:Real-Time Polymerase Chain Reaction; D012083:Renin / Q000378:metabolism*; D012084:Renin-Angiotensin System; D017673:Sodium Chloride, Dietary / Q000009:adverse effects; D015854:Up-Regulation
chemical_list: D017673:Sodium Chloride, Dietary; D000808:Angiotensinogen; D000804:Angiotensin II; D012083:Renin