The Effects Of High-salt Diet On Blood Pressure And Kidney And The Interventional Impact Of Telmisartan In Wistar Rats

Objective:To observe the effects of high-salt diet on blood pressure and kidney and the intervention of telmisartan. Methods:Wistar rats were randomly divided into normal control group (given 0.5% NaCl), high salt model group (given 8% NaCl) and the intervention group (given 8% NaCl+telmisartan). The blood pressure of rat was assessed by the tail artery pressure. Meantime, high salt model group was divided into model hypertension group and model normal blood pressure group. After 23 weeks, calculated clearance rate and the renal hypertrophy index followed by carotid artery pressure measurement were performed. HE and MAS SON staining were used respectively to detect the kidney morphology and the renal fibrosis. The urine was collected to determine the level of Na+, K+, albumin, total protein and creatinin. The content of superoxide dismutase (SOD) and malondialdehyde (MDA) and the activity of Na+-K+-ATP enzyme and Ca2+-ATP enzyme were assessed by spectrophotography and the content of angiotensinⅡ(AngⅡ) was detected by radio-immunoassay. The mRNA expression of peroxisome proliferator-activated receptor y (PPARy), nuclear factor-kappB (NF-κB), transforming growth factor-β1 (TGF-(31), kidney injury molecule-1 (Kim-1) was measured through real-time RT-PCR. Western blot assay was performed to detect the protein level of PPARy, NF-κB and TGF-β1. Results:Compared with normal control group, the blood pressure in model group increased (P<0.01). Telmisartan significantly attenuated high salt diet-induced renal damage. Compared with normal control group, in model and intervention group albumin and the ratio of Na+and K+increased (P<0.01) and the creatinin decreased (P<0.01). Moreover, the total urine protein in model hypertension group was much higher than other groups (P<0.05). The levels of SOD and Ca2+-ATP enzyme in model group were lower than normal control group. Furthermore, the contetnt of AngⅡand the activity of Na+-K+-ATP enzyme in model hypertension group were also lower than normal control group (P<0.01). The mRNA expression of Kim-1 in model group increased compared with normal control group (P<0.05). The protein level of PPARy and TGF-β1 in model group was much higher than normal control group. Compared with model group, telmisartan significantly attenuated high salt diet-induced increase of TGF-β1 protein expression (P<0.05). Conclusion:1. Long-term high-salt diet could induce high blood pressure in rats,2. High salt diet could be independent on high blood pressure to cause renal damage,3. the possible mechanism underlying high salt diet-induced high blood pressure was related to the decreased sodium pump activity and renal damage was closely associated with oxidative stress besides high blood pressure,4. telmisartan attenuated high salt diet-induced high blood pressure and renal damage and the inhibition of TGF-β1 expression was involved in telmisartan-mediated protection against renal damage,5.The renal damage in model hypertension group was more severe than in model normal blood pressure group.