Objectives: Renal dysfunctional metabolism of sodium or potassium play a key role in formation of salt sensitivity. The aim was to investigate alteration of gene in kidney of Dahl rat and preliminaryly explore the protective mechanism of potassium on blood pressure, which would shed some new light in future. Methods: Male Dahl sensitive rats and 13BN-SS rats were randomly divided into nornal salt group, high salt group and high salt plus potassium supplement group respectively; Illumina RatRef-12 Expression BeadChip were used for screening the renal different genes between high salt group and high salt plus potassium supplement group, and the clusters, GO, Pathway analysis of functionally related genes were determined on the basis of their annotation term co-occurrence; qRT-PCR was performed to validate the gene expression data; Results: Microarray scanning had shown that 594 different gene were obtained between highsalt group and high salt plus potassium supplement group in Dahl salt sensitive rats; there were 429 upregulated genes and 479 downregulated genes between Dahl salt sensitive rats and13BN-SS rat in high salt group,; Dietary high saltcould increase the expression of SGK1 in Dahl salt sensitive rats, in contrast, potassium supplement could reverse this phenomenon; the expression of Mcoln3 was higher in Dahl salt sensitive ratsthan 13BN-SS rat, morever, potassium supplement could upregulate the expressionof Mcoln3 in Dahl salt sensitive rats and 13BN-SS rat. Conclusion: Dietary high salt could increase the expression of SGK1 in Dahl salt sensitive rats, in contrast, potassium supplement could reverse this phenomenon, which may be associated with the protective effect of potassium. Abnormality of the expression of Mcoln3 may be involved in salt-induced elevation of blood pressure in Dahl salt sensitive rat