Inhibition of nitric oxide synthesis potentiates the responsiveness of carotid chemoreceptors to systemic hypoxia in the rat.

Carotid sinus nerve afferent activity was recorded in the peripheral end of the cut carotid sinus nerves in rats anesthetized with urethane, paralyzed and artificially ventilated with pure oxygen in order to abolish any resting chemoreceptor activity. Hypoxic stimuli were applied by switching pure oxygen to a nitrogen/oxygen gas mixture in the inspiratory line, reducing end-tidal oxygen concentrations to 10% FETO2, 8% FETO2 and 6% FETO2 respectively. Each stimulus was applied for 60 s and ventilation was switched again to pure oxygen. Increases in the carotid sinus nerve activities were due to chemo- and not to baroreceptor stimulation as arterial blood pressure decreased during hypoxia. After administration of nitric oxide synthase blocker L-NG-nitroarginine methyl ester, 30 mg/kg weight i.v., chemoreceptor excitatory response to all hypoxic stimuli increased significantly. Subsequent administration of L-arginine, 300 mg/kg weight i.v., restored chemoreceptor response to hypoxia to initial magnitude. It is concluded that NO is generated in the carotid body and attenuates chemoreceptor responsiveness in rats in vivo, as reported on isolated carotid bodies in cats in vitro.