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Skeletal muscle regulates extracellular potassium

Authors :
McDonough, Alicia A.
Thompson, Curtis B.
Youn, Jang H.
Source :
The American Journal of Physiology. June, 2002, Vol. 282 Issue 6, pF967, 8 p.
Publication Year :
2002

Abstract

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

Details

ISSN :
00029513
Volume :
282
Issue :
6
Database :
Gale General OneFile
Journal :
The American Journal of Physiology
Publication Type :
Academic Journal
Accession number :
edsgcl.87774585