Abstract P300: Blood Pressure Increase Upon High Dietary Potassium Supplementation Is Not Associated With Renal Sodium Retention Or Plasma Volume Expansion

• Published in: Hypertension (Dallas, Tex. 1979) Tex. 1979), 2023-09, Vol.80 (Suppl_1)
• Main Authors: Ehmke, Heimo, Vitzthum, Helga, Steffen, Philine, Marx, Christian, Ewald, Jan, Morhenn, Karoline M, Seniuk, Anika
• Format: Article
• Language: English
• ISSN: 0194-911X; 1524-4563
• DOI: 10.1161/hyp.80.suppl_1.P300

Abstract only Background: High dietary K + supplementation increases arterial blood pressure in humans and in mice. The mechanisms underlying this unexpected response are still not fully understood. Recent studies in mice reported an activation of the epithelial sodium channel (ENaC) suggesting that renal Na + retention may prominently contribute to the blood pressure increase caused by a high KCl intake. Here, we tested whether a high K + intake causes renal Na + retention and plasma volume expansion. Methods: Na + -replete C57BL/6J mice were subjected to either a normal (0.93%, NK) or a high (5%, HK) KCl or KCitrate diet for up to 14 days. Blood pressure responses to diets and to the additional administration of the ENaC blocker amiloride were measured using radiotelemetry in unrestrained animals. Plasma aldosterone concentrations were quantified by ELISA. Renal Na + retention was assessed by determining urinary Na + excretion. To detect plasma volume expansion, we used a dilution method (Evans blue), determined blood hematocrit, and estimated end diastolic left ventricular volume by echocardiography after 10 days of diet. Results: Both high K + diets increased arterial blood pressure selectively in the dark phase by a nearly identical extent (ΔMAP dark: HKCl +12.7±2.3 mm Hg, p=0.0045, HKCit +12.1±3.0 mm Hg, p=0.0211; ΔMAP light: HKCl -0.2±1.5 mm Hg, p>0.9999, HKCit +2.4±2.2 mm Hg, p=0.9692, 1-way ANOVA, n=7). Even though plasma aldosterone levels were markedly elevated (HKCl 9.9-fold, p=0.0001, HKCit 4.6-fold, p=0.0116, 1-way ANOVA, n=11-12), neither a reduction of renal Na + excretion (urinary [Na + ]/[creatinine] NK 1.0±0.14, HKCl 1.40±0.23, p=0.3873, HKCit 0.94±0.20, p0.9999, HKCit 870±62 μl, p>0.9999, 1-way ANOVA, n=6-13) was detected upon the two high K + diets. Amiloride did not normalize arterial blood pressure in mice fed a HKCl or HKCit diet (ΔMAP dark: HKCl +1.2±2.3 mm Hg, p=0.6391 HKCit +2.8±2.0 mm Hg, p=0.2472, 2-tailed paired t-test, n=4). Conclusions: Our findings indicate that excessive K + intake causes elevated blood pressure independent of renal Na + retention and volume expansion in Na + -replete mice.