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MEMBRANE TRANSPORTERS, ION CHANNELS, AND PUMPS

AMPK activation with AICAR provokes an acute fall in plasma [K⁺]

¹Department of Physiology and Biophysics, University of Southern California Keck School of Medicine, ²Department of Anatomy-Physiology and Lipid Research Unit, Laval University Hospital Research Centre, Quebec, Canada

Submitted 4 October 2007 ; accepted in final form 12 November 2007

AMP-activated protein kinase (AMPK), activated by an increase in intracellular AMP-to-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 5-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside (AICAR) infusion: 38.4 mg/kg bolus then 4 mg·kg^–1·min^–1 infusion. Plasma [K⁺] and [glucose] both dropped at 1 h of AICAR infusion and [K⁺] dropped to 3.3 ± 0.04 mM by 3 h, 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 and 180 min AICAR infusion. In mice expressing a dominant inhibitory form of AMPK in the 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.

potassium homeostasis; sodium-potassium-ATPase; muscle; urine

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