title: [Expression and role of soluble epoxide hydrolase in renal tissue of two kidneys one clip  hypertension rats model].
abstract: OBJECTIVE
  To investigate renal expression of soluble epoxide hydrolase (sEH) in 2-kidney-1-clip rats  and explore the role of sEH in renal arterial stenosis hypertensive development.
  
  
  METHODS
  Hypertensive models  were established in Sprague-Dawly rats by chronic partial occlusion of left renal artery. In the study,16 male  Sprague-Dawly rats were randomized into sham operation group and 2-kidney-1-lip (2K1C) group (n=8, each  group), and were observed for 40 days. Before operation and every ten days after operation, systolic blood  pressure (SBP) was measured and twenty-four-hour urine was collected. At the end of the observation, the  blood and kidneys were harvested. The serum Na,24-hour urine protein excretion were measured. Renin activity  and angiotensin II concentrition in plasm and renal tissue were evaluated by radioimmunoassay (RIA).The expression  of sEH, peroxisome proliferator-activated receptor-γ (PPARγ) in kidneys were assessed by immunohistochemistry  and Western blotting. Histology was analysed after kidney sections were stained by Grocott-Gomori methenamine-silver nitrate.
  
  
  RESULTS
  After surgery, the systolic blood pressure in 2K1C group gradually became higher than  that in sham group. Urine protein excretion was statistically increased in 2K1C group on the 30 th and 40 th  days, while serum sodium was of no significant difference from those of the two groups. Renin-angiotensin system  in both clipped and nonclipped kidneys were also invoked by the 2K1C surgery. Both sEH and PPARγ were  upregulated in renocortex and renomedulla in 2K1C group. The two groups were compared: in SBP,on the 10 th day,  (106.70±7.71) vs.(124.04±6.79) mmHg, P<0.001,and on the 40 th day,(107.80±10.01) vs. (150.40±11.76) mmHg,  P<0.001; Urine protein excretion,on the 30 th day,(206.81±37.61)vs.(292.33±20.53)mg/d, P=0.005; Serum  sodium, (179.76±29.20) vs. (157.72±51.00)mmol/L, P=0.44; Renin activity[plasm(50.00±13.66) vs.(132.90± 31.22)ng/(L×h),P=0.03; clipped kidney(128.40±36.88)vs.(324.90±56.66)ng/(g×h), P=0.01; nonclipped  kidney(103.00±19.87)vs.(345.10±42.68)ng/(g×h), P<0.001]; Ang II [plasm(4 810.00±1 164.00)vs. (10 470.00±1 760.00) ng/L,P=0.02, clipped kidney(735.90±154.40)vs.(2 094.00±372.20)ng/g, P=0.005, nonclipped  kidney(648.10±217.90)vs.(1 774.00±206.60)ng/g, P=0.002]; the expression of sEH (sEH/β-actin) in  renocortex [clipped kidney (0.33±0.08) vs. (1.73±0.12), P<0.001, nonclipped kidney (0.43±0.09)vs. (0.70± 0.05), P=0.04]; the expression of PPARγ (PPARγ/β-actin) in renocortex [clipped kidney(0.17±0.05) vs.  (0.89±0.11), P=0.002, and nonclipped kidney(0.27±0.07) vs. (0.56±0.07), P=0.04]. Clipped kidney showed more  severe glomerulosclerosis and tubular atrophy in 2K1C group than in sham group.
  
  
  CONCLUSIONS
  sEH probably plays an  important role in the development of hypertension in the rat models of renovascular hypertension. The activation  of PPAR-γ and RAAS by renal arterial stenosis are associated with sEH upregulation, suggesting that they might  regulate sEH expression and take part in hypertensive development.
authors.affiliation: Department of Nephrology, Peking University Third Hospital, Beijing 100191, China.
authors.forename: Yue-juan
authors.initials: YJ
authors.lastname: Pan
authors.forename: Zhong-fei
authors.initials: ZF
authors.lastname: Tao
authors.forename: Qian
authors.initials: Q
authors.lastname: Wang
authors.forename: Min
authors.initials: M
authors.lastname: Lu
authors.forename: You-fei
authors.initials: YF
authors.lastname: Guan
authors.forename: Yi
authors.initials: Y
authors.lastname: Zhu
authors.forename: Yue
authors.initials: Y
authors.lastname: Wang
mesh_terms: D000818:Animals; D004851:Epoxide Hydrolases / Q000378:metabolism* / Q000502:physiology; D006978:Hypertension, Renovascular / Q000201:enzymology* / Q000503:physiopathology*; D007668:Kidney / Q000201:enzymology* / Q000503:physiopathology; D008297:Male; D047495:PPAR gamma / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D012084:Renin-Angiotensin System / Q000502:physiology
chemical_list: D047495:PPAR gamma; D004851:Epoxide Hydrolases