Insulin stimulates active sodium transport in toad bladder by two mechanisms

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 drugs^6–8. We have now examined the mechanisms by which insulin increases short circuit current (a measure of active sodium transport) in the toad bladder.