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  • Title: The ouabain receptor in animal tissues and its endogenous ligand.
    Author: Lichtstein D, Samuelov S, Deutsch J, Xu H, Lutz RA, Chernick SS, Chernick SS.
    Journal: Klin Wochenschr; 1987; 65 Suppl 8():40-8. PubMed ID: 3037184.
    Abstract:
    Cardiac glycosides bind to the Na+,K+-ATPase and inhibit its activity. Low concentrations (less than 10(-7) M) of ouabain stimulate the activity of Na+,K+-ATPase in whole homogenates of rat brain. The magnitude of this stimulation varies from 5 to 70%. The concentration of ouabain which induces maximal stimulation is also highly variable and ranges between 10(-9) to 10(-7) M. This stimulation may be explained by the presence of an endogenous ouabain-like compound (OLC) in the brain homogenate. Mammalian tissues and body fluids including brain, heart, kidney, plasma, urine and cerebrospinal fluid contain a unidentified OLC. An endogenous OLC was also demonstrated in toad skin and plasma. This compound was purified to homogeneity and identified using UV, NMR and Mass spectroscopies to be 3-hydroxy-14, 15-epoxy-20,22-dienolide glycoside (resibufogenin). Several reports have suggested that unsaturated fatty acids are the ouabain-like regulators of the Na+,K+-ATPase. Furthermore, Saline infusion to WKY rats, which was shown to increase OLC in the plasma causes also an elevation of free fatty acids. Thus, the interaction of fatty acids with several plasma membrane components was studied. Ouabain binding, opiate binding and binding to the beta-adrenergic receptor were all inhibited by micromolar concentrations of the unsaturated fatty acids, linoleic, oleic and arachidonic. Binding to the opiate receptor was inhibited with IC50 of 40-90 microM and binding to beta-adrenergic receptor with IC50 of 350-450 microM.(ABSTRACT TRUNCATED AT 250 WORDS)
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