Recent advances in understanding integrative control of potassium homeostasis.
Recent advances in understanding integrative control of potassium homeostasis.
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DOI：
10.1146/annurev.physiol.010908.163241
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发表时间：
2009
影响因子：
18.2
通讯作者：
McDonough AA
中科院分区：
文献类型：
--
作者：
Youn JH;McDonough AA
钾稳态系统受到非常严格的调节。最近的研究揭示了负责这种严格控制的传感和分子机制。除了由细胞外液 (ECF) [K+] 增加介导的经典反馈调节之外，还有证据表明存在前馈机制：肠道中感知到膳食 K+ 摄入量，并且激活一种未识别的肠道因子以刺激肾脏 K+ 排泄。该途径可以解释肾脏和肾外对 K+ 摄入量变化的反应，这些反应独立于 ECF [K+] 的变化而发生。禁食或 K+ 剥夺期间保存 ECF K+ 的机制已有描述：肾脏 NADPH 氧化酶激活引发级联反应，引发 K+ 通道从细胞膜上收缩，肌肉对细胞 K+ 摄取的胰岛素刺激产生抵抗。这些机制是如何由 K+ 剥夺触发的仍不清楚。细胞 AMP 激酶依赖性蛋白激酶活性引发 K+ 从 ECF 到 ICF 的急性转移，这在运动或缺血中可能很重要。这些最新进展可能揭示高钾饮食对心血管系统的有益影响。
The potassium homeostatic system is very tightly regulated. Recent studies have shed light on the sensing and molecular mechanisms responsible for this tight control. In addition to classic feedback regulation mediated by a rise in extracellular fluid (ECF) [K+], there is evidence for a feedforward mechanism: Dietary K+ intake is sensed in the gut, and an unidentified gut factor is activated to stimulate renal K+ excretion. This pathway may explain renal and extrarenal responses to altered K+ intake that occur independently of changes in ECF [K+]. Mechanisms for conserving ECF K+ during fasting or K+ deprivation have been described: Kidney NADPH oxidase activation initiates a cascade that provokes the retraction of K+ channels from the cell membrane, and muscle becomes resistant to insulin stimulation of cellular K+ uptake. How these mechanisms are triggered by K+ deprivation remains unclear. Cellular AMP kinase–dependent protein kinase activity provokes the acute transfer of K+ from the ECF to the ICF, which may be important in exercise or ischemia. These recent advances may shed light on the beneficial effects of a high-K+ diet for the cardiovascular system.