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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在小鼠缺钾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 ⁺ ] 由肾脏和骨骼肌的适应性维持，此前对这些反应分别进行了研究。我们旨在确定这些器官系统如何协同工作以保持雄性 C57BL/6J 小鼠的ECF [K ⁺ ] 喂食 K ⁺缺乏饮食 (0K) 与 1% K ⁺饮食 (1K) 10 天（n = 5- 6/组）。在 0K 喂养期间，血浆 [K ⁺ ] 从 4.5 mM 降至 2 mM；后肢肌肉（腓肠肌和比目鱼肌）损失了 28 mM K ⁺（从 115 ± 2 到 87 ± 2 mM）并获得了 27 mM Na ⁺（从 27 ± 0.4 到 54 ± 2 mM）。肌肉组织加倍 [Na ⁺] 与其他人报道的炎症、细胞因子产生或高血压无关。通过免疫印迹评估，0K 与 1K 喂养小鼠中肌肉转运蛋白的适应性包括钠泵 a2-b2 亚基减少、K ⁺ - Cl ^- - 协同转运蛋白同种型 3 减少和磷酸化 (p) Na ⁺ -K ⁺ -2 Cl 增加^-协同转运蛋白同种型 1 (NKCC1p)、Ste20/SPS-1 相关的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。肾转运蛋白的适应，使 K ⁺减少 98%排泄，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 ⁺输送至上皮 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，在喂食 0K 的 10 天后，小鼠从尿液中流失了约 48 mmol K ⁺，并且肌肉将约 47 mmol K ⁺从 ICF 转移到 ECF，这说明了 K ⁺缺乏期间协同反应的重要性。