<p>Hypertension is a risk factor for cardiovascular disease. Low dietary potassium (K⁺) intake is associated with higher blood pressure (BP) and increased activity of the kidney NaCl cotransporter NCC. Increasing dietary K⁺ can lower NCC activity and reduce BP, but a threshold for beneficial effects of dietary K⁺ is apparent, with very high K⁺ intakes associated with higher BP. Here, we examine in male C57Bl/6J mice if an optimal BP-lowering K⁺ intake window exists and the molecular basis of K⁺ driven increases in BP. Telemetric BP recordings are performed in mice receiving diets with normal (0.74%) NaCl content and progressively increasing K⁺ content (0.75% to 5% K⁺, as KCl) for 5 days. None of the diets examined reduce BP despite lowering NCC activity and above 1.75% K⁺ intake systolic BP (SBP) is raised, concurrent with higher aldosterone and sodium channel (αENaC) activity. On a high NaCl diet (1.57% Na⁺), K⁺-driven increases in αENaC and SBP are absent and high NaCl does not increase SBP. We conclude that the higher BP subsequent to excess K⁺ intake is aldosterone and ENaC-dependent, and increased dietary K⁺ is beneficial when Na⁺ intake is high.</p>