Subject(s)
4-Nitrophenylphosphatase/metabolism , Kidney Cortex/enzymology , Kidney Medulla/enzymology , Phosphoric Monoester Hydrolases/metabolism , Potassium/pharmacology , Sodium-Potassium-Exchanging ATPase/metabolism , Adenosine Triphosphate/pharmacology , Adrenalectomy , Animals , Dexamethasone/administration & dosage , Enzyme Activation/drug effects , Male , Ouabain/pharmacology , Rats , Sodium/pharmacologySubject(s)
Dexamethasone/administration & dosage , Kidney Cortex/enzymology , Kidney Medulla/enzymology , Sodium-Potassium-Exchanging ATPase/metabolism , 4-Nitrophenylphosphatase/metabolism , Adrenalectomy , Animals , Body Weight/drug effects , DNA/metabolism , Enzyme Activation/drug effects , Female , Kinetics , RNA/metabolism , RatsABSTRACT
The mechanism of activation of renal Na+-K+-ATPase was studied in rats 2 wk after unilateral nephrectomy. The increase in enzyme specific activity was confined to the outer medulla and occurred without changes in the cellular contents of RNA or protein. Enzyme activation was accompanied by increases in the levels of the phosphorylated intermediate with little or no change in the apparent turnover numbers of the reaction. The specific activity of the ouabain-sensitive p-nitrophenylphosphatase also increased by uninephrectomy but to a larger extent than did Na+-K+-ATPase. Kinetic studies demonstrated an increase in Vmax for ATP, sodium, and potassium, and small increases in Km for ATP and K1/2 for potassium. There was no change in the activation energies or phase transition temperature to indicate alterations in the membrane environment of Na+-K+-ATPase. Adrenalectomy did not adversely affect activation. These results indicate that activation of renal Na+-K+-ATPase after reduction of renal mass occurs mainly by an increase in the number of sodium pump sites.
Subject(s)
Kidney/enzymology , Kidney/physiology , Sodium-Potassium-Exchanging ATPase/metabolism , Adenosine Triphosphate , Animals , Enzyme Activation , Kinetics , Male , Nephrectomy , Potassium , Rats , SodiumABSTRACT
The mechanism of activation of Na+-K+-ATPase after chronic potassium loading has been investigated in the rat kidney. Potassium loading stimulated the specific activity of Na+-K+-ATPase in the cortex and medulla of the kidney. This effect was not accompanied by a generalized increase in the cellular contents of RNA and proteins and could not be accounted for by an effect of potassium loading on renal growth. Enzyme induction does not appear to be mediated by changes in the endogenous levels of glucocorticoid or thyroid hormones. Evidence obtained from investigation of the partial reactions (Pi intermediate, ouabain-sensitive pNPPase) of the Na+-K+-ATPase enzymatic reaction is consistent with the interpretation that chronic potassium loading in the rat increases the number of enzyme units (Na+ pumps) in the cortex of the kidney. Analysis of the kinetic parameters (Km, K1/2, Vmax, Hill coefficients) of the enzymatic reaction indicates that K+ loading has little or no effect on the kinetic properties (affinity, cooperativity) of the stimulated transport enzyme.
