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Am J Physiol Renal Physiol 282: F967-F974, 2002; doi:10.1152/ajprenal.00360.2001
0363-6127/02 $5.00
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Vol. 282, Issue 6, F967-F974, June 2002

INVITED REVIEW
Skeletal muscle regulates extracellular potassium

Alicia A. McDonough, Curtis B. Thompson, and Jang H. Youn

Department of Physiology and Biophysics, University of Southern California Keck School of Medicine, Los Angeles, California 90089-9142

Maintaining extracellular fluid (ECF) K+ concentration ([K+]) within a narrow range is accomplished by the concerted responses of the kidney, which matches K+ excretion to K+ intake, and skeletal muscle, the main intracellular fluid (ICF) store of K+, which can rapidly buffer ECF [K+]. In both systems, homologous P-type ATPase isoforms are key effectors of this homeostasis. During dietary K+ deprivation, these P-type ATPases are regulated in opposite directions: increased abundance of the H,K-ATPase "colonic" isoform in the renal collecting duct drives active K+ conservation while decreased abundance of the plasma membrane Na,K-ATPase alpha 2-isoform leads to the specific shift of K+ from muscle ICF to ECF. The skeletal muscle response is isoform and muscle specific: alpha 2 and beta 2, not alpha 1 and beta 1, levels are depressed, and fast glycolytic muscles lose >90% alpha 2, whereas slow oxidative muscles lose ~50%; however, both muscle types have the same fall in cellular [K+]. To understand the physiological impact, we developed the "K+ clamp" to assess insulin-stimulated cellular K+ uptake in vivo in the conscious rat by measuring the exogenous K+ infusion rate needed to maintain constant plasma [K+] during insulin infusion. Using the K+ clamp, we established that K+ deprivation leads to near-complete insulin resistance of cellular K+ uptake and that this insulin resistance can occur before any decrease in plasma [K+] or muscle Na+ pump expression. These studies establish the advantage of combining molecular analyses of P-type ATPase expression with in vivo analyses of cellular K+ uptake and excretion to determine mechanisms in models of disrupted K+ homeostasis.

sodium, potassium-adenosine triphosphatase; hydrogen, potassium-adenosine triphosphatase; potassium clamp; hypokalemia; ion homeostasis


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