The Na-Cl cotransporter NCC is expressed in the distal convoluted tubule, activated by phosphorylation, and has been implicated in renal NaCl and K⁺ homeostasis. The serum and glucocorticoid inducible kinase 1 (SGK1) contributes to renal NaCl retention and K⁺ excretion, at least in part, by stimulating the epithelial Na⁺ channel and Na⁺-K⁺-ATPase in the downstream segments of aldosterone-sensitive Na⁺/K⁺ exchange. In this study we confirmed in wild-type mice (WT) that dietary NaCl restriction increases renal NCC expression and its phosphorylation at Thr⁵³, Thr⁵⁸, and Ser⁷¹, respectively. This response, however, was attenuated in mice lacking SGK1 (Sgk1^−/−), which may contribute to impaired NaCl retention in those mice. Total renal NCC expression and phosphorylation at Thr⁵³, Thr⁵⁸, and Ser⁷¹ in WT were greater under low- compared with high-K⁺ diet. This finding is consistent with a regulation of NCC to modulate Na⁺ delivery to downstream segments of Na⁺/K⁺ exchange, thereby modulating K⁺ excretion. Dietary K⁺-dependent variation in renal expression of total NCC and phosphorylated NCC were not attenuated in Sgk1^−/− mice. In fact, high-K⁺ diet-induced NCC suppression was enhanced in Sgk1^−/− mice. The hyperkalemia induced in Sgk1^−/− mice by a high-K⁺ diet may have augmented NCC suppression, thereby increasing Na⁺ delivery and facilitating K⁺ excretion in downstream segments of impaired Na⁺/K⁺ exchange. In summary, changes in NaCl and K⁺ intake altered NCC expression and phosphorylation, an observation consistent with a role of NCC in NaCl and K⁺ homeostasis. The two maneuvers dissociated plasma aldosterone levels from NCC expression and phosphorylation, implicating additional regulators. Regulation of NCC expression and phosphorylation by dietary NaCl restriction appears to involve SGK1.