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Title: Up-regulation of intrarenal renin-agiotensin system contributes to renal damage in high-salt induced hypertension rats. Author: Wu H, Liang Y, Zheng Y, Bai Q, Zhuang Z, A L, Zheng D, Wang Y. Journal: Kidney Blood Press Res; 2014; 39(6):526-35. PubMed ID: 25531334. Abstract: BACKGROUND/AIMS: To investigate the change of intrarenal renin-agiotensin system (RAS) and its role in high-salt induced hypertension. METHODS: Wistar rats were divided into normal-salt (NS), high-salt diet (HS) and high-salt diet with Losartan group (HS+L), for 6 weeks. Systolic blood pressure (SBP) was monitored. Blood and urine samples were collected every 2 weeks. Angiotensinogen (AGT) was measured by ELISA. AGT mRNA and protein were measured by real-time PCR and immunohistochemistry. Renin activity and angiotensin II (Ang II) were measured by radioimmunoassay. RESULTS: HS versus NS group, SBP increased from 2(nd) week (P<0.05), urinary protein increased at 6(th) week (P<0.05). Although plasma renin, AGT and Ang II had no significant changes (P>0.05), renal cortex renin, AGT, and Ang II increased significantly in HS (P<0.05). In HS+L, Losartan failed to reduce SBP (P>0.05) but abolished the increase of proteinuria (P<0.01), renal cortex renin, AGT, Ang II and urinary AGT reduced (P<0.05) while plasma renin, AGT and Ang II enhanced (P<0.05) when compared with HS. Urinary AGT was positively correlated with renal AGT (r=0.592, P <0.01) and Ang II (r=0.726, P <0.01). CONCLUSION: Inappropriate response of the renal RAS to a high salt diet may contribute to hypertension and renal damage, and urinary AGT could reflect intrarenal RAS activity.[Abstract] [Full Text] [Related] [New Search]