Change of the renal hydrogen sulfide system in salt-sensitive hypertensive rats
10.3760/cma.j.issn.2095-428X.2014.13.012
- VernacularTitle:高盐饮食诱导Dah1大鼠高血压模型肾脏内源性硫化氢体系的变化
- Author:
Pan HUANG
;
Suxia WANG
;
Yali REN
;
Chaoshu TANG
;
Junbao DU
;
Hongfang JIN
- Publication Type:Journal Article
- Keywords:
High salt;
Hypertension;
Dah1 salt-sensitive rat;
Hydrogen sulfide
- From:
Chinese Journal of Applied Clinical Pediatrics
2014;29(13):997-1000
- CountryChina
- Language:Chinese
-
Abstract:
Objective To study the change of the renal endogenous hydrogen sulfide (H2 S) pathway in the development of salt-sensitive hypertension in Dah1 rats.Methods Sixteen male Dah1 rats,in accordance with the random number table,were randomly divided into control group and high salt group fed with diet containing 80 g/kg NaCl.After 8 weeks,24 h urine sodium,24 h urinary protein,serum creatinine and serum urea were measured.The microstructural and ultrastructural changes in kidney were observed with light microscope and electronic microscope.The serum and kidney H2S contents were determined by using sulphur-sensitive electrode method.The mRNA levels of cystathionine β-synthase(CBS),cystathionine γ-lyase(CSE) and mercaptopyruvate sulfurtransferase(MPST) in renal tissue were determined by means of real-time polymerase chain reaction(RT-PCR).The protein expressions of CBS,CSE and MPST in renal tissue were detected by using Western blot.Results Compared with control group,high salt group rats had a significant rise in blood pressure,declined renal function,damaged renal structure,segmental glomerular sclero sis,small artery wall thickening,and occlusion of the lumen.Moreover,the endogenous H2S pathway in kidney of Dah1rats with high salt diet was downregulated markedly,demonstrated by the decreased serum and kidney H2S content,the reduced renal CBS,CSE and MPST mRNA expressions and CBS protein expression of kidney tissue.Conclusion The endogenous H2S/CBS pathway is downregulated during the development of salt-sensitive hypertension in Dah1 rats.
