期刊
ANNUAL REVIEW OF PHYSIOLOGY
卷 71, 期 -, 页码 381-401出版社
ANNUAL REVIEWS
DOI: 10.1146/annurev.physiol.010908.163241
关键词
dietary potassium; potassium adaptation; potassium excretion; kidney; muscle; insulin
类别
资金
- NIDDK NIH HHS [R01 DK057678] Funding Source: Medline
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R01DK057678] Funding Source: NIH RePORTER
The potassium homeostatic system is very tightly regulated. Recent studies have shed light on the sensing and molecular mechanisms responsible for this fight control. hi 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.
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