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The effects of infusions of ouabain on chemoreceptor activity recorded from the peripheral end of a sectioned carotid sinus nerve were studied in cats anaesthetized with pentobarbitone. Ouabain caused a marked increase in chemoreceptor discharge followed by a decline in discharge to frequencies near or below the pre-ouabain level; during the latter period further administration of ouabain had no effect. Infusion of ouabain during hypoxia further increased the chemoreceptor discharge, but this effect was short-lasting. On intracarotid administration ouabain was less effective in cats with the ganglioglomerular (sympathetic) nerves cut, whereas on intravenous administration no significant difference was observed. Following intravenous administration of ouabain the chemoreceptor peak discharge occurred with dose levels similar to those needed to cause cardiac arrhythmias, but following intracarotid administration the chemoreceptor discharge peaked at doses about 40% of those causing arrhythmias. During ouabain-induced excitation the stimulatory action of NaCN, CO2-equilibrated Locke solution and acetylcholine was potentiated, as was the chemo-inhibition induced by dopamine. During the post-excitatory period the responses evoked by these substances were reduced or abolished. Neither mecamylamine, a nicotinic antagonist, nor physostigmine, an anti-cholinesterase, affected the response of the carotid chemoreceptors to ouabain. The major finding of this study was that ouabain initially 'sensitizes' the carotid body chemoreceptors and then 'desensitizes' them. The most likely mechanism responsible for these effects is the well established Na+--K+-ATPase-inhibiting property of ouabain.