Short-term regulation of the proximal tubule Na+,K+-ATPase: increased/decreased Na+,K+-ATPase activity mediated by protein kinase C isoforms.
In different species and tissues, a great variety of hormones modulate Na+,K+-ATPase activity in a short-term fashion. Such regulation involves the activation of distinct intracellular signaling networks that are often hormone- and tissue-specific. This minireview focuses on our own experimental observations obtained by studying the regulation of the rodent proximal tubule Na+,K+-ATPase. We discuss evidence that hormones responsible for regulating kidney proximal tubule sodium reabsorption may not affect the intrinsic catalytic activity of the Na+,K+-ATPase, but rather the number of active units within the plasma membrane due to shuttling Na+,K+-ATPase molecules between intracellular compartments and the plasma membrane. These processes are mediated by different isoforms of protein kinase C and depend largely on variations in intracellular sodium concentrations.
Pedemont
C H
CH
Department of Pharmacological and Pharmaceutical Sciences, College of Pharmacy, University of Houston, Texas 77204-5515, USA. pedemonte@uh.edu
Bertorello
A M
AM
D000818:Animals; D002478:Cells, Cultured; D004298:Dopamine / Q000378:metabolism; D004789:Enzyme Activation / Q000502:physiology; D007687:Kidney Tubules, Proximal / Q000201:enzymology*; D009893:Opossums; D010766:Phosphorylation; D020033:Protein Isoforms / Q000235:genetics*; D011493:Protein Kinase C / Q000235:genetics / Q000378:metabolism*; D051381:Rats; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism*
D020033:Protein Isoforms; D011493:Protein Kinase C; D000254:Sodium-Potassium-Exchanging ATPase; D004298:Dopamine