October 1964
Volume 3, Issue 5
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Articles  |   October 1964
Studies on Sodium-Potassium Activated Adenosinetriphosphatase
Author Affiliations
  • SJOERD L. BONTING
    Ophthalmology Branch, National Institute of Neurological Diseases and Blindness, National Institutes of Health Bethesda, Md., Department of Ophthalmology and the Oscar Johnson Institute, Washington University School of Medicine, St. Louis, Mo.
  • BERNARD BECKER
    Ophthalmology Branch, National Institute of Neurological Diseases and Blindness, National Institutes of Health Bethesda, Md., Department of Ophthalmology and the Oscar Johnson Institute, Washington University School of Medicine, St. Louis, Mo.
Investigative Ophthalmology & Visual Science October 1964, Vol.3, 523-533. doi:
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      SJOERD L. BONTING, BERNARD BECKER; Studies on Sodium-Potassium Activated Adenosinetriphosphatase . Invest. Ophthalmol. Vis. Sci. 1964;3(5):523-533.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Ouabain was injected into the vitreous humor of one eye of rabbits in doses of 0.1, 0.2 and 0.5 mcg. Aqueous humor inflow in the injected eye was inhibited significantly 49, 51, and 78 per cent, respectively, in these three dose groups 4 to 5 days after injection. In vitro Na-K activated ATPase activity of the ciliary body was inhibited significantly by 24, 16, and 27 per cent, corresponding to an in vivo enzyme inhibition of 70 per cent at the highest dose level. Within each dose group there was a significant, positive correlation between inhibition of aqueous humor inflow and in vitro Na-K activated ATPase inhibition. There was also close similarity in the change with time of both inhibitions, with maximum effects at 4 to 5 days after injection and return to normal after 20 days. 86Rb accumulation in the ciliary body-iris preparation in vitro was inhibited to the same extent as aqueous inflow and estimated in vivo enzyme inhibition. These observations support the rate-limiting role of ciliary body Na-K activated ATPase in aqueous humor formation via the control of active cation transport.

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