Relation between Na-K-ATPase activity and respiratory rate in the rat kidney.
The relation between Na-k-ATPase activity in homogenates of rat kidney and oxygen consumption in kidney slices was studied by employing different physiological maneuvers known to change the activity of renal Na-K-ATPase. Treatment of euthyroid rats with 3,5,3'-triiodo-1-thyronine increased Na-K-ATPase activity, sodium-dependent oxygen consumption (QO2[t]), and para-aminohippurate (PAH) accumulation by kidney slices without changing glomerular filtration rate or net sodium reabsorption by the intact kidney. Treatment with methylprednisolone also increased Na-K-ATPase, QO2[t], and PAH transport. Chronic potassium loading, on the other hand, increased renal Na-K-ATPase to the same degree as the first two procedures, but QO2[t] and PAH accumulation were unchanged. Partial nephrectomy induced an increase in the activity of Na-K-ATPase in homogenates of the remaining kidney fragment, but QO2[t] did not change significantly and PAH uptake was unaltered. An increase in the activity of Na-K-ATPase in kidney homogenates is therefore not necessarily associated with a parallel change in oxygen consumption by the intact cell.
D000251:Adenosine Triphosphatases / Q000378:metabolism*; D000618:Aminohippuric Acids / Q000378:metabolism; D000818:Animals; D005919:Glomerular Filtration Rate / Q000187:drug effects; D007668:Kidney / Q000378:metabolism*; D007672:Kidney Cortex / Q000201:enzymology / Q000378:metabolism*; D007679:Kidney Medulla / Q000201:enzymology / Q000378:metabolism*; D008297:Male; D008775:Methylprednisolone / Q000494:pharmacology; D010101:Oxygen Consumption / Q000187:drug effects; D011188:Potassium / Q000494:pharmacology; D051381:Rats; D012964:Sodium / Q000378:metabolism; D014284:Triiodothyronine / Q000494:pharmacology
D000618:Aminohippuric Acids; D014284:Triiodothyronine; D012964:Sodium; D000251:Adenosine Triphosphatases; D011188:Potassium; D008775:Methylprednisolone