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 sodium channel and Na⁺/K⁺-ATPase in the downstream segments of aldosterone-sensitive Na⁺/K⁺ exchange. Here 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 (-/-), 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.