| With the aging of our population and changing lifestyles, the prevalence of hypertension increased year by year. Long-term hypertension can lead to hypertensive renal damage, if not active intervention, eventually may lead to chronic renal failure. Good blood pressure control is undoubtedly the basis for containment of hypertensive renal impairment, but in recent years, despite the extensive use of drugs with high blood pressure, high blood pressure caused by the incidence of end-stage renal disease but growing. U.S. epidemiological data shows that since 1981-2001 due to hypertensive renal damage persuaded to enter the number of patients increased by nearly eight times, second only to diabetic nephropathy, it is estimated that by 2030 there will be more than 2 million ESRD patients need dialysis treatment not only costly, and the 5-year survival rate is only guilty of% of hypertension caused by chronic kidney disease (chronickidneydisease, CKD) has become an important cause of dialysis patients, hypertension is the prognosis of patients with chronic kidney disease, a major risk factor. Therefore, early detection, diagnosis, and control of blood pressure, prevention of hypertensive renal damage, delay the occurrence and development of ESRD as an important clinical issue. Renin angiotensin aldosterone system (renin an angiotensin 1 aldosteronesysystem, RAAS) play a significant role, RAAS by regulating extracellular fluid volume, to maintain sodium balance and the role of regulating cardiovascular function involved in the maintenance of hemodynamic stable. Hemodynamic stability. Early studies suggest that angiotensinⅡ(angiotensinⅡ, AngⅡ) is involved in RAAS in hypertension and target organ damage in the main material, aldosterone (aidosterone, ALD) is a hypertensive renal damage caused by one of the factors, combined with its receptor through hemodynamic and direct cellular effects induced fibrosis play a role.Podocyte membrane holes now that the molecular structure and function is to maintain the glomerular filtration barrier of the main factors, nephrin protein in which one of the important proteins, was found that the lack of nephrin may cause glomerular sclerosis. This study compared the RAAS system blockade on blood pressure in spontaneously hypertensive rats and the combination of renal protection.MethodExperimental groups:five 12 week old male Wistar-Kyoto (WKY) rats as the control group (A group),30 12 weeks of age in spontaneously hypertensive rats (SHR) were divided into hypertensive group (B group) and ramipril treatment group (C group), telmisartan treatment group (D group), Eplerenone treated group (E group), ramipril and Eplerenone combined treatment group (F group),5 only.Gastric lavage drugs:eplerenone and telmisartan combined treatment group (G group). A group B group was given drinking water for, C group with the ramipril group [2.5 mg/(kg·d)] ig, D group with telmisartan [10mg/(kg·d)] Irrigation stomach, E group with Eplerenones [100mg/(kg·d)] ig, F group with Eplerenone group [50 mg/ (kg·d)]+ramipril group [1.125 mg/(kg·d)] ig, G group with Eplerenones [50 mg/ (kg·d)]+telmisartan [5mg/(kg·d)] ig. A total of 8 weeks.Measure blood pressure:0,4,8 weeks of experiment method using sets of tail blood pressure.Sample preparation and pathological changes:in the 8th week, rats were killed, preparation kidney specimens were detected by immunohistochemistry kidney nephrin protein., HE staining, detection of renal biopsy and the scores, the degree of kidney damage. By electron microscopy kidney podocyte pathological changes. All data are expressed. Statistical comparison between groups by analysis of variance (ANOVA) and Bonferroni multiple comparison test was after. Result1. Systolic blood pressure (SBP)B group compared with blood pressure to group A gradually increased (P<0.05). C, D, E, F and G in blood pressure, and B to F,G were the most significant (P<0.01)2. Kidney damageLight microscope, A group of glomeruli, tubules without pathological changes, B group the greatest degree of damage, C, D, E, F, G group than the B group to reduce glomerular lesions to G were the most obvious.3. The nephrin, podocyte damage levelsBy electron microscopy, group B podocyte changes, the biggest nephrin expression is A group was significantly lower than pathological damage, A group B group, nephrin expression is significantly higher than that of group B (P< 0.05).Immunohistochemical observations on foot, nephrin expression is A group of group B, the treatment group was significantly lower nephrin can increase the protein expression level, with the most obvious, G F increased (P< 0.01).Conclusion1 RASS antagonist in spontaneously hypertensive rats were function, in combination with eplereone joint ramipril group or joint telmisartan group is the most obvious function.2 RASS antagonist in spontaneously hypertensive rats with kidney pathological damage, according to eplereone joint ramipril group or joint telmisartan renal protection is the most obvious group.3 RASS antagonist in spontaneously hypertensive rats kidney nephrin podocyte protein expression level has effect, according to eplereone joint ramipril group or joint telmisartan group nephrin protein expression than other treatment group.
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