Abstract
Diphenylhydantoin has been shown to have no effect on the rate of sodium efflux in resting or stimulated lobster nerves. The drug reduces sodium influx in stimulated nerves by 40% but has no effect upon sodium influx in resting nerves. These results are consistent with the view that the drug acts primarily by limiting the increase in sodium permeability which occurs during stimulation; they are inconsistent with the theory that the drug acts by stimulating the sodium-potassium pump. A review of some of the chemical and physiological data concerning the effects of diphenylhydantoin on a variety of tissues supports this hypothesis.
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