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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-s a lt 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<sup>nd</sup> week ( P <0.05), urinary protein increased at 6<sup>th</sup> 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.

Up-Regulation of Intrarenal Renin-Agiotensin System Contributes to Renal Damage in High-Salt Induced Hypertension Rats