Abstract: Objective To investigate the impact of high-salt intake on epithelial-to-mesenchymal transition（EMT）and renal fibrosis in Dahl salt-sensitive（SS）rats. Methods Twenty-four male SS and twelve consomic SS-13BN（13BN）rats were randomized to low-salt or high-salt diets for 4and 8weeks,respectively. After the intervention,systolic blood pressure（SBP）and biochemical markers in blood and urine were measured,and renal fibrosis was evaluated by Masson staining. The mRNA and protein expression levels of E-cadherin and alpha smooth muscle actin（α-SMA）were assessed by immunohistochemistry and real-time polymerase chain reaction（PCR）. Results Compared with baseline levels,the high-salt diet groups showed significantly higher blood pressure,the increase being more obvious in the SS high-salt diet groupSS:（184.4±4.5）vs（139.0±0.3）mm Hg;13BN:（156.3±2.1）vs（139.8±1.2）mm Hg. SS rats had significantly increased SBP after 8 weeks of high-salt diets relative to 4weeks（227.1±3.6）vs（184.4±4.5）mm Hg,P＜0.01. After 4weeks of salt loading,Masson staining of collagen in kidneys was more pronounced in rats with high-salt diets than with normal diets. Under high-salt feeding,SS rats showed higher glomerular and interstitial fibrosis than 13 BN rats glomeruli:（9.8±1.9）% vs（8.7±0.4）%;interstitium:（9.1±0.2）% vs（6.7±0.3）%. SS rats with high-salt diets had more collagen deposition in the glomeruli and interstitium at 8weeks than at 4weeksglomeruli:（15.4±0.9）% vs（9.8±1.9）%;interstitium:（13.9±0.4）% vs（9.1±0.2）%. High-salt feeding induced tubular EMT as identified by reduced expression of E-cadherin and increased expression ofα-SMA in SS rats after 4and 8weeks of high-salt feeding. Renal interstitial fibrosis was correlated negatively with E-cadherin,but positively withα-SMA（r=-0.720 for E-cadherin;r=0.848forα-SMA;both P＜0.01）. Conclusion High-salt intake might induce tubular EMT and facilitate renal fibrosis in salt-sensitive rats.