We characterized mouse blood pressure and ion transport in the setting of commonly used rodent diets that drive K⁺ intake to the extremes of deficiency and excess. Male 129S2/Sv mice were fed either K⁺-deficient, control, high-K⁺ basic, or high-KCl diets for 10 days. Mice maintained on a K⁺-deficient diet exhibited no change in blood pressure, whereas K⁺-loaded mice developed an ~10-mmHg blood pressure increase. Following challenge with NaCl, K⁺-deficient mice developed a salt-sensitive 8 mmHg increase in blood pressure, whereas blood pressure was unchanged in mice fed high-K⁺ diets. Notably, 10 days of K⁺ depletion induced diabetes insipidus and upregulation of phosphorylated NaCl cotransporter, proximal Na⁺ transporters, and pendrin, likely contributing to the K⁺-deficient NaCl sensitivity. While the anionic content with high-K⁺ diets had distinct effects on transporter expression along the nephron, both K⁺ basic and KCl diets had a similar increase in blood pressure. The blood pressure elevation on high-K⁺ diets correlated with increased Na⁺-K⁺-2Cl^- cotransporter and γ-epithelial Na⁺ channel expression and increased urinary response to furosemide and amiloride. We conclude that the dietary K⁺ maneuvers used here did not recapitulate the inverse effects of K⁺ on blood pressure observed in human epidemiological studies. This may be due to the extreme degree of K⁺ stress, the low-Na⁺-to-K⁺ ratio, the duration of treatment, and the development of other coinciding events, such as diabetes insipidus. These factors must be taken into consideration when studying the physiological effects of dietary K⁺ loading and depletion.

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