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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.

Effects of extreme potassium stress on blood pressure and renal tubular sodium transport