Effects Of High Salt Diet On Wistar Rats Blood And Left Ventricular Remodeling And The Intervention Of Telmisartan

Objective:(1) To investigate the role of inflammatory factor-induced hypertension and (or) left ventricular remodeling. (2) to evaluate the effects of telmisartan on this model and further explore the corresponding mechanisms. Methods:60 Wistar rats were randomly divided into normal control group, high salt (8%) model group and high salt+ telmisartan group. The tail artery pressure was determined every 2 weeks. After 24 weeks, high salt model group was divided into model hypertension (MH) group and model normal pressure (MN) group. Color dopplar ultrasound was used to detect the structure and function of the heart. The left ventricle was collected for the measurement of LVMI. The myocardial cell diameter and the area of interstitial fibrosis were respectively measured through HE and Masson staining. The content of SOD and MDA and the activity of ATPase in the blood and tissue were assessed by spectrophotography, the content of AngⅡand TNF-αwere detected by radio-immunoassay. ELISA was performed for the measurement of CRP in the blood. The expression of NF-κB p65, TGF-β1 and PPARγin the heart were determined by Real-Time RT-PCR and western blot analysis, respectively. Results:The blood pressure of MH group was higher than other groups (P< 0.05). Compared with normal control group, the LVMI, the myocardial cell diameter and the interstitial fibrosis area in MH and MN groups increased (P< 0.05). Moreovre, LVPw in MH group was thicker than other groups (P< 0.05). The content of Ang II in MH group was little higher than MN group. Compared with normal control group, in MH and MN groups, the level of SOD increased in the blood and decreased in the tissue (P<0.05) and the content of CRP significantly increased (P<0.05) but there was no difference in the measurement of ATPase activity, MDA and TNF-αlevels. Compared with normal control group, the mRNA expression of NF-κB p65, TGF-β1 in MH and MN groups increased and the treatment of telmisartan could attenuate this increase. However, the mRNA expression of PPARγin MN group decreased compared with normal control group. Furthermore, telmisartan significantly inhibited the increased protein expression of TGF-β1 in MH and MN groups. Conclusions:(1) high salt diet could induce the hypertension of rats. (2) high salt diet might be independent on hypertension to cause left ventricular remodeling. (3) local inflammation and oxidatie stress might involve in high salt diet-induced hypertension and (or) left ventricular remodeling. (4) the possible mechanisms of telmisartan-mediated protection against high salt diet-induced hypertension and (or) left ventricular remodeling might be partly due to inhibiting the expression of p65, producing the anti-inflammatory effects and attenuating the oxidative stress.