Sodium transport defect of ouabain-resistant renal Na,K-ATPase.
The murine renal Na,K-ATPase is resistant to cardiac glycosides. It is not yet known however whether altered active transport is associated with the drug-resistance. To investigate this problem Na,K-ATPases were purified from the outer medulla of both rat and rabbit kidneys and reconstituted identically into liposomes. The Na-stimulation of the Na,K-ATPase activity before reconstitution and of the Na-transport after reconstitution was measured. A Na-defect inherent in the ouabain-resistant rat Na,K-ATPase was discovered indicating a link between the cardiac glycoside sensitivity and the Na-transport.
Anner
B M
BM
Department of Pharmacology, Geneva University Medical Center, Switzerland.
Imesch
E
E
Moosmayer
M
M
D000818:Animals; D001693:Biological Transport, Active; D004351:Drug Resistance; D007668:Kidney / Q000201:enzymology*; D007700:Kinetics; D008081:Liposomes; D008861:Microsomes / Q000201:enzymology; D010042:Ouabain / Q000494:pharmacology*; D011817:Rabbits; D051381:Rats; D012964:Sodium / Q000378:metabolism*; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism*; D013045:Species Specificity
D008081:Liposomes; D010042:Ouabain; D012964:Sodium; D000254:Sodium-Potassium-Exchanging ATPase