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Microsomal Na+-stimulated NADH-cytochrome c reductase: could it be involved in sodium transport?

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Luisier,  A.L.
Department of Physiology, Max Planck Institute of Biophysics, Max Planck Society;
Département de Chirurgie Expérimentale, Hôpital Cantonal Universitaire, CH-1011, Lausanne, (Switzerland);

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Robinson,  J.W.L.
Department of Physiology, Max Planck Institute of Biophysics, Max Planck Society;
Département de Chirurgie Expérimentale, Hôpital Cantonal Universitaire, CH-1011, Lausanne, (Switzerland);

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Kinne,  Rolf
Department of Physiology, Max Planck Institute of Biophysics, Max Planck Society;
Département de Chirurgie Expérimentale, Hôpital Cantonal Universitaire, CH-1011, Lausanne, (Switzerland);

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Citation

Luisier, A., Robinson, J., & Kinne, R. (1974). Microsomal Na+-stimulated NADH-cytochrome c reductase: could it be involved in sodium transport? Experientia, 30(6), 631-633. doi:10.1007/BF01921513.


Cite as: https://hdl.handle.net/21.11116/0000-0009-E43E-1
Abstract
During the last few years, there has been much discussion about the possibility of the existence of more than one sodium pump in absorbing epithelia. The most convincing evidence has been obtained with kidney proximal tubular cells but research with various different epithelial cells has suggested that the dichotomy is widespread. One of the weak points of the hypothesis remains the fact that, whereas it is generally accepted that sodium-for-potassium exchange is mediated by a (Na+ + K+)-stimulated ATPase, no indication has been forthcoming as to the biochemical nature of the second pump. A plausible candidate for such a mechanism appeared to be afforded by the Na+-stimulated NADH- cytochrome c reductase system of microsomal fractions, first described by Siekevitz. The present preliminary survey was undertaken in an attempt to discover any link between this enzyme and the sodium-pumping system of the kidney. Of the various criteria listed by Skou for the identification of an enzyme system with a pumping mechanism, we have concentrated on its cytological location, its sensitivity towards cationic stimulation, and its behaviour with respect to inhibitors, and we have concluded regretfully that this enzyme is probably not responsible for sodium transport across cell membranes in epithelial cells, and its physiological function remains a mystery.