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1 Physiology and Biophysics, USC Keck School of Medicine, Los Angeles, California, United States
2 Department of Anatomy-Physiology, Laval University Hospital Research Centre, Quebec, Canada
3 Los Angeles, California, United States; Physiology and Biophysics, USC Keck School of Medicine, Los Angeles, California, United States
* To whom correspondence should be addressed. E-mail: mcdonoug{at}usc.edu.
AMP activated protein kinase (AMPK), activated by an increase in intracellular AMP:ATP ratio, stimulates pathways that can restore ATP levels. We tested the hypothesis that AMPK activation influences extracellular fluid (ECF) K+ homeostasis. In conscious rats, AMPK was activated with AICAR (5-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside) infusion: 38.4 mg/kg bolus then 4 mg/kg/min infusion. Plasma [K+] and [glucose] both dropped at 1h of AICAR infusion, [K+] dropped to 3.3 ± 0.04 mM by 3 hr, linearly related to the increase in muscle AMPK phosphorylation. AICAR treatment did not increase urinary K+ excretion. AICAR lowered [K+] whether plasma [K+] was chronically elevated or lowered. The K+ infusion rate needed to maintain baseline plasma [K+] reached 15.7 ± 1.3 µmol K+ kg-1 min-1 between 120 - 180 min AICAR infusion. In mice expressing a dominant inhibitory form of AMPK in muscle (Tg-KD1) baseline [K+] was not different from controls (4.2 ± 0.1 mM), but the fall in plasma [K+] in response to AICAR (0.25 g/kg) was blunted: [K+] fell to 3.6 ± 0.1 in controls and to 3.9 ± 0.1 mM in Tg-KD1 suggesting that ECF K+ redistributes, at least in part to muscle ICF. In summary, these findings illustrate that activation of AMPK activity with AICAR provokes a significant fall in plasma [K+] and suggest a novel mechanism for redistributing K+ from ECF to ICF.
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