Extracellular fluid (ECF) [K⁺] is maintained by adaptations of kidney and skeletal muscle, responses heretofore studied separately. We aimed to determine how these organ systems work in concert to preserve ECF [K⁺] in male C57BL/6J mice fed a K⁺ deficient diet (0K) versus 1% K⁺ diet (1K) for 10 days (n=5-6/group). During 0K feeding, plasma [K⁺] fell from 4.5 to 2 mM; hindlimb muscle (gastrocnemius and soleus) lost 28 mM K⁺ (from 115 ± 2 to 87 ± 2 mM) and gained 27 mM Na⁺ (from 27 ± 0.4 to 54 ± 2 mM). Doubling of muscle tissue [Na⁺] was not associated with inflammation, cytokine production or hypertension as reported by others. Muscle transporters' adaptations in 0K vs. 1K fed mice, assessed by immunoblot, included decreased sodium pump a2-b2 subunits, decreased K⁺- Cl^-- cotransporter isoform 3, and increased phosphorylated (p) Na⁺-K⁺-2 Cl^- cotransporter isoform 1 (NKCC1p), Ste20/SPS-1 related proline-alanine rich kinase (SPAKp) and oxidative stress responsive kinase 1 (OSR1p) consistent with intracellular fluid (ICF) K⁺ loss and Na⁺ gain. Renal transporters' adaptations, effecting a 98% reduction in K⁺ excretion, included 2-3-fold increased phosphorylated Na⁺-Cl^- cotransporter (NCCp), SPAKp and OSR1p abundance, limiting Na⁺ delivery to epithelial Na⁺ channels where Na⁺ reabsorption drives K⁺ secretion; renal K sensor Kir 4.1 abundance fell 25%. Mass balance estimations indicate that over 10 days of 0K feeding, mice lose ~48 mmol K⁺ into the urine and muscle shifts ~47 mmol K⁺ from ICF to ECF, illustrating the importance of the concerted responses during K⁺ deficiency.

中文翻译：

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在小鼠 K+ 缺乏饮食期间协调骨骼肌和肾脏的适应以调整细胞外 [K+]。


细胞外液 (ECF) [K ⁺ ] 通过肾脏和骨骼肌的适应来维持，迄今为止的反应是单独研究的。我们的目的是确定这些器官系统如何协同工作，以在喂食缺乏 K ⁺饮食 (0K) 与 1% K ⁺饮食 (1K) 的雄性 C57BL/6J 小鼠中保持 ECF [K ⁺ ] 10 天 (n=5- 6/组）。在 0K 喂养期间，血浆 [K ⁺ ] 从 4.5 降至 2 mM；后肢肌肉（腓肠肌和比目鱼肌）损失 28 mM K ⁺ （从 115 ± 2 到 87 ± 2 mM）并增加 27 mM Na ⁺ （从 27 ± 0.4 到 54 ± 2 mM）。正如其他人报道的那样，肌肉组织 [Na ⁺ ] 的倍增与炎症、细胞因子产生或高血压无关。通过免疫印迹评估，0K 与 1K 喂养小鼠的肌肉转运蛋白适应性包括钠泵 a2-b2 亚基减少、K ⁺ - Cl ^- - 协同转运蛋白亚型 3 减少和磷酸化 (p) Na ⁺ -K ⁺ -2 Cl 增加^-协同转运蛋白亚型 1 (NKCC1p)、Ste20/SPS-1 相关富含脯氨酸丙氨酸激酶 (SPAKp) 和氧化应激反应激酶 1 (OSR1p) 与细胞内液 (ICF) K ⁺损失和 Na ⁺增加一致。肾脏转运蛋白的适应性，导致 K ⁺排泄减少 98%，包括磷酸化 Na ⁺ -Cl ^-协同转运蛋白 (NCCp)、SPAKp 和 OSR1p 丰度增加 2-3 倍，限制 Na ⁺输送到上皮 Na ⁺通道，其中 Na ⁺重吸收驱动K ⁺分泌；肾K传感器Kir 4.1丰度下降25%。 质量平衡估计表明，经过 10 天的 0K 喂养，小鼠通过尿液损失了约 48 mmol K ⁺ ，肌肉将约 47 mmol K ⁺从 ICF 转移到 ECF，这说明了 K ⁺缺乏期间协调反应的重要性。