Abstract: Objective: To test the hypothesis that in a high-salt induced hypertension in normal rats, whether the changes of intrarenal renin-agiotensin system (RAS) play a critical role in renal damage and could be reflected by urinary angiotensinogen (AGT). Methods: In the study, 27 normotensive male Wistar-Kyoto rats were divided into control group ［0.3% (mass faction) NaCl in chow, n=9, NS］, high-salt diet group ［8% (mass faction) NaCl in chow, n=9, HS］ and high-salt diet with Losartan group ［8% (mass faction) NaCl in chow and 20 mg/（kg·d） Losartan in gavages, n=9, HS+L)］, and were fed for six weeks. The blood pressure was monitored and urine samples were collected every 2 weeks. AGTs in plasma, kidney and urine were measured by ELISA kits. The renal cortex expression of mRNA and protein of AGT were measured by Real-time PCR and immunohistochemistry (IHC). The renin activity and ANGⅡ were measured by radioimmunoassay (RIA) kits. Results: Compared with NS, the systolic blood pressure (SBP) ［(156±2) mmHg vs. (133±3) mmHg, P<0.05］ increased significantly at the end of the 2nd week, and the urinary protein ［(14.07±2.84) mg/24 h vs. (7.62±3.02) mg/24 h, P<0.05］ increased significantly at the end of the 6th week in HS. Compared with HS, there was no significant difference in SBP (P>0.05) but the proteinuria ［(9.69±2.73) mg/24 h vs. (14.07±2.84) mg/24 h, P<0.01］ decreased significantly in HS+L. Compared with NS, there was no significant difference in the plasma renin activity, angiotensinogen and ANGⅡ level in HS (P>0.05), but the renal cortex renin content ［(8.72±1.98) ng/(mL·h) vs. (4.37±1.26) ng/(mL·h), P<0.05］, AGT formation ［(4.02±0.60) ng/mg vs. (2.59±0.42) ng/mg, P<0.01］, ANGⅡ level ［(313.8±48.76) pmol/L vs. (188.9±46.95) pmol/L, P<0.05］ were increased significantly in HS, and the urinary AGT and ANGⅡ excretion rates increased significantly (P<0.05). Compared with HS, the plasma renin activity, angiotensinogen and ANGⅡ level were significantly increased (P<0.05), but the renal cortex renin content, AGT formation, ANGⅡ level significantly decreased (P<0.05), and the urinary AGT and ANGⅡ excretion rates decreased significantly in HS+L (P<0.05). The urinary AGT excretion rates were positively correlated with the AGT level in the renal cortex (P<0.05). Conclusion: Up-regulation of intarenal RAS may contribute to renal damage in high-salt induced hypertension rats. Urinary AGT may reflect the status of intrarenal RAS.

Key words: Sodium chloride, dietary, Renin-agiotensin system, Hypertension, Proteinuria, Angiotensinogen