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Abstract: FR-PO594

Effects of Extreme Dietary Potassium Restriction and K+ Loading on Blood Pressure and Renal Tubular Na+ Transport

Session Information

Category: Fluid and Electrolytes

  • 901 Fluid and Electrolytes: Basic

Authors

  • Boyd-Shiwarski, Cary R., University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, United States
  • Beacham, Rebecca T., University of Pittsburgh, Pittsburgh, Pennsylvania, United States
  • Weaver, Claire J., University of Florida, Oviedo, Florida, United States
  • Shiwarski, Daniel J., Carnegie Mellon University, Pittsburgh, Pennsylvania, United States
  • Connolly, Kelly, University of Pittsburgh, Pittsburgh, Pennsylvania, United States
  • Marciszyn, Allison L., University of Pittsburgh, Pittsburgh, Pennsylvania, United States
  • Subramanya, Arohan R., University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, United States
Background

For almost a century it has been known that dietary potassium intake inversely correlates with blood pressure. Yet, it is unclear how potassium restriction leads to hypertension, or how potassium excess causes a natriuresis despite elevated aldosterone levels. Our goal was to study the effects of dietary potassium on blood pressure, acid/base balance, and ion transport.

Methods

Wild-type SV129 mice were fed K+ deficient, control, high K+ basic, and high KCl diets for 10 days. We monitored BP using radiotelemetry probes, urine electrolyte excretion via metabolic cages, and transporter expression via immunofluorescence, western blots, and diuretic challenges.

Results

Interestingly, despite the induction of hypokalemia, extreme K+ depletion had no effect on blood pressure. In contrast, K+ loading resulted in a progressive ~10 mmHg increase in blood pressure. To determine whether these effects were dependent on NaCl intake, we challenged mice with 1% saline. The K+ deficient mice developed an increase in blood pressure (~8 mmHg), whereas K+ replete mice exhibited no significant change in blood pressure with saline challenge. Notably, just 10d of K+ restriction was associated with diabetes insipidus, evidenced by polyuria and a decrease in AQP2 expression. This was associated with an increase in sodium transporters in the upstream tubule, likely the cause of salt sensitivity. The elevated blood pressure on the K+ loaded diet correlated with elevated aldosterone levels and increased ENaC activation. During K+ loading, the type of anion (basic vs. chloride-rich) had a considerable effect on key transporters along the tubule, despite no differences on blood pressure.

Conclusion

In our model, the effect of dietary K+ on blood pressure was linked to NaCl intake, due to differential effects of K+ loading and restriction on sodium transport pathways along the nephron. The inverse relationship between dietary K+ intake and blood pressure was only observed in the setting of NaCl loading, though our data strongly suggest that AQP2 expression should be closely monitored to accurately interpret such results. Further, the accompanying anionic content should be taken into consideration when modeling the physiologic effect of K+ intake on tubular salt transport and blood pressure.

Funding

  • NIDDK Support