Abstract: PO1086
High Dietary Potassium Increases Blood Pressure in a Rat Model of CKD
Session Information
- Fluid, Electrolyte, and Acid-Base Disorders: Basic
November 04, 2021 | Location: On-Demand, Virtual Only
Abstract Time: 10:00 AM - 12:00 PM
Category: Fluid, Electrolyte, and Acid-Base Disorders
- 901 Fluid, Electrolyte, and Acid-Base Disorders: Basic
Authors
- Gritter, Martin, Erasmus MC, Rotterdam, Zuid-Holland, Netherlands
- Wei, Kuangyu, Erasmus MC, Rotterdam, Zuid-Holland, Netherlands
- Danser, Alexander H., Erasmus MC, Rotterdam, Zuid-Holland, Netherlands
- Vogt, Liffert, Amsterdam UMC Locatie AMC, Amsterdam, North Holland, Netherlands
- De Borst, Martin H., Universitair Medisch Centrum Groningen, Groningen, Groningen, Netherlands
- Hoorn, Ewout J., Erasmus MC, Rotterdam, Zuid-Holland, Netherlands
- Rotmans, Joris I., Leids Universitair Medisch Centrum, Leiden, Zuid-Holland, Netherlands
Background
Potassium dephosphorylates the sodium chloride cotransporter (pNCC) thereby increasing natriuresis and reducing blood pressure. However, it is unclear if this response is intact in chronic kidney disease (CKD).
Methods
To address this, CKD was induced by 5/6th nephrectomy in rats which were fed a low KCl diet (0.03%), normal KCl diet (0.1%), modestly high KCl diet (0.8%), high KCl diet (2.5%) or high KCitrate diet (2.5%). The latter group was included to analyze the effect of the accompanying anion. All diets contained 0.16% Na+. The effects of these diets on telemetric blood pressure, plasma potassium (K+), plasma aldosterone, plasma bicarbonate, and pNCC were analyzed.
Results
Both the low and the high KCl diets increased blood pressure compared to the normal KCl diet, although the effect of the high KCl diets was more pronounced (Table). Higher dietary K+ intake caused higher plasma aldosterone levels, and high KCitrate further increased plasma aldosterone. pNCC was significantly increased by the low KCl diet and decreased by the moderately high KCl diet. The effect of dietary KCl on pNCC, however, was lost with the high KCl diet. The high KCitrate diet attenuated the rise in blood pressure despite the highest plasma aldosterone and pNCC levels.
Conclusion
Although the inverse relationship between potassium and pNCC is intact in experimental CKD, high potassium diets cause hypertension possibly mediated by aldosterone. This rise in blood pressure is attenuated when potassium is given with citrate, despite high aldosterone and pNCC levels.
| Low KCl diet | Normal KCl diet | Moderately high KCl diet | High KCl diet | High KCitrate diet | |
| Δ Systolic BP, mmHg | 3* | Ref. | 9* | 21* | 8* |
| Plasma K+, mEq/L | 2.3* | 3.8 | 4.5 | 5.2 | 5.0 |
| Plasma aldosterone, ng/L | N.M. | 33 | 186* | 577* | 1144* |
| Plasma bicarbonate, mEq/L | 18.9 | 22.0 | 19.7 | 18.8 | 35.2* |
| Urine K+, mEq/24h | 0.2 | 0.3 | 3.1* | 9.8* | 9.7* |
| Urine Na+, mEq/24h | 1.0 | 1.0 | 1.6* | 1.7* | 1.6* |
| pNCC expression, A.U | 2.9* | 1 | 0.3* | 0.9 | 15* |
* P < 0.01 compared to normal KCl diet (ANOVA with post-hoc testing). A.U., arbitrary units; BP, blood pressure; N.M., not measured.