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 e nd of the cut carotid sinus nerves in rats anesthetized with urethane, paralyzed and artificially ventilated with pure oxygen in order to ab olish any resting chemoreceptor activity. Hypoxic stimuli were applied by switching pure oxygen to a nitrogen/oxygen gas mixture in the insp iratory line, reducing end-tidal oxygen concentrations to 10% FET(O2), 8% FET(O2) and 6% FET(O2) 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 baror eceptor stimulation as arterial blood pressure decreased during hypoxi a. After administration of nitric oxide synthase blocker L-N-G-nitroar ginine methyl ester, 30 mg/kg weight i.v., chemoreceptor excitatory re sponse to all hypoxic stimuli increased significantly. Subsequent admi nistration of L-arginine, 300 mg/kg weight i.v., restored chemorecepto r response to hypoxia to initial magnitude. It is concluded that NO is generated in the carotid body and attenuates chemoreceptor responsive ness in rats in vivo, as reported on isolated carotid bodies in cats i n vitro.