Abstract
INSULIN has been shown to increase sodium and potassium fluxes in a series of tissues including muscle1, and colon2 and the isolated perfused kidney3. Attempts to define the exact mechanisms by which insulin stimulates ion transport in these tissues have been hindered by their anatomical complexity and heterogeneous cell populations. Tracer flux studies, using 22Na, in frog muscle1 and toad bladder4 have suggested a direct stimulatory action of insulin on the sodium pump. Preincubation of intact frog muscle with insulin for 1 h has been shown to increase the amount of ouabain binding by this tissue suggesting that insulin unmasks latent sodium pumps in this structure5. The urinary bladder of the toad (Bufo marinus) has been shown to transport sodium actively from the urinary (mucosal) side to the blood (serosal) side and has been used extensively to study cation transport and the effects and mode of action of numerous hormones and drugs6–8. We have now examined the mechanisms by which insulin increases short circuit current (a measure of active sodium transport) in the toad bladder.
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WIESMANN, W., SINHA, S. & KLAHR, S. Insulin stimulates active sodium transport in toad bladder by two mechanisms. Nature 260, 546–547 (1976). https://doi.org/10.1038/260546a0
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DOI: https://doi.org/10.1038/260546a0
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