The giant axons of this extreme osmoconformer were adapted, in vitro, to progressive hyposmotic dilution of the bathing medium (from 1024 m-Osmol to concentrations as low as 76.8 m-Osmol). Hyposmotic adaptation is associated with reductions in the intracellular concentrations of both sodium and potassium ions. These reductions do not appear to result from appreciable axonal swelling. The different electrical responses to isosmotic and hyposmotic dilution suggest that reduction in [Na+]1 results from ouabain-dependent sodium extrusion, in response to ionic dilution, and that reduction in [K+]1 is induced by a combination of ionic and osmotic dilution. The reduced level of intracellular potassium achieved during hyposmotic adaptation represents a balance between the necessity to contribute to osmotic equilibration and to maintain a potassium gradient across the axon membrane sufficient to produce appreciable axonal hyperpolarization during dilution of the bathing medium. This hyperpolarization tends to maintain the amplitude of the action potential, by compensating for reduction in overshoot (with decline in ENa), and by reducing sodium inactivation. This, together with the reduction in [Na+]1, enables overshooting action potentials of relatively large amplitude and rapid rise time to be maintained during more than tenfold dilution of the ionic and osmotic concentration of the bathing medium.
How Hyperpolarization and the Recovery of Excitability Affect Propagation through a Virtual Anode in the Heart
