A network of kinases, including WNKs, SPAK and Sgk1, is critical for the independent regulation of K⁺ and Na⁺ transport in the distal nephron. Angiotensin II is thought to act as a key hormone in orchestrating these kinases to switch from K⁺ secretion during hyperkalaemia to Na⁺ reabsorption during intravascular volume depletion, thus keeping disturbances in electrolyte and blood pressure homeostasis at a minimum. It remains unclear, however, how K⁺ and Na⁺ transport are regulated during a high Na⁺ intake, which is associated with suppressed angiotensin II levels and a high distal tubular Na⁺ load. We therefore investigated the integrated blood pressure, renal, hormonal and gene and protein expression responses to large changes of K⁺ intake in Na⁺ replete mice. Both low and high K⁺ intake increased blood pressure and caused Na⁺ retention. Low K⁺ intake was accompanied by an upregulation of the sodium‐chloride cotransporter (NCC) and its activating kinase SPAK, and inhibition of NCC normalized blood pressure. Renal responses were unaffected by angiotensin AT1 receptor antagonism, indicating that low K⁺ intake activates the distal nephron by an angiotensin‐independent mode of action. High K⁺ intake was associated with elevated plasma aldosterone concentrations and an upregulation of the epithelial sodium channel (ENaC) and its activating kinase Sgk1. Surprisingly, high K⁺ intake increased blood pressure even during ENaC or mineralocorticoid receptor antagonism, suggesting the contribution of aldosterone‐independent mechanisms. These findings show that in a Na⁺ replete state, changes in K⁺ intake induce specific molecular and functional adaptations in the distal nephron that cause a functional coupling of renal K⁺ and Na⁺ handling, resulting in Na⁺ retention and high blood pressure when K⁺ intake is either restricted or excessively increased.