During hypovolemia and hyperkalemia, the kidneys defend homeostasis by sodium retention and potassium secretion, respectively. Aldosterone mediates both effects, but it is unclear how the same hormone can evoke such different responses. To address this, we mimicked hypovolemia and hyperkalemia in four groups of rats with a control diet, low sodium diet, high potassium diet or a combined diet. The low sodium and combined diets increased plasma and kidney angiotensin II. The low sodium and high potassium diets increased plasma aldosterone to a similar degree (3-fold), while the combined diet increased aldosterone to a greater extent (10-fold). Despite similar sodium intake and higher aldosterone, the high potassium and combined diets caused a greater natriuresis than the control and low sodium diets, respectively (p<0.001 for both). This potassium-induced natriuresis was accompanied by a decreased abundance but not phosphorylation of the sodium chloride cotransporter (NCC). In contrast, the epithelial sodium channel (ENaC) increased in parallel with aldosterone showing the highest expression with the combined diet. The high potassium and combined diets also increased WNK4, but decreased Nedd4-2 in the kidney. Total and phosphorylated SPAK were also increased but were retained in the cytoplasm of distal convoluted tubule cells. In summary, high dietary potassium overrides the effects of angiotensin II and aldosterone on NCC to deliver sufficient sodium to ENaC for potassium secretion. Potassium may inhibit NCC through WNK4 and help activate ENaC through Nedd4-2.