Hypoxic excitation of medullary vasomotor neurons in rats are not mediated by glutamate or nitric oxide.

Ischemic-hypoxic neuro-excitation and toxicity have been attributed to a rapid release of glutamate and formation of nitric oxide. We have now demonstrated that sympatho-excitatory response (1.2-fold increase in sympathetic nerve activity) induced by intratracheal administration of 100% N2 for 20 s in anesthetized rats and membrane inward currents (0.4-0.5 nA) induced by cyanide (300 microM) and hypoxia (saturated with 75% N2) of these neurons recorded in slices of rat rostral ventrolateral medulla were neither reduced by blocking glutamate receptors with kynurenate, synaptic transmission with tetrodotoxin nor by inhibiting nitric oxide synthase with N-nitro-L-arginine, indicating that glutamate, synaptic inputs, and nitric oxide are not involved in rapid responses of reticulospinal vasomotor neurons to hypoxia.