SODIUM-NITROPRUSSIDE BLOCKS THE CAT CAROTID CHEMOSENSORY INHIBITION INDUCED BY DOPAMINE, BUT NOT THAT BY HYPEROXIA

We studied the effects of the nitric oxide (NO) synthase inhibitor, N omega-nitro-L-arginine methyl ester (L-NAME), and the NO donor, sodium nitroprusside (SNP) on cat chemosensory responses to intravenous inje ctions of NaCN (0.1-100 mu g/kg) and dopamine (0.1-20 mu g/kg), and to hyperoxic ventilation (100% O-2, 60-120 s). Cats were anesthetized wi th sodium pentobarbitone, paralyzed and artificially ventilated to pre vent secondary ventilatory effects. The frequency of chemosensory disc harges (f(x)) was recorded from one sectioned carotid sinus nerve. L-N AME (50 mg/kg i.v.) increased basal f(x) and slightly potentiated the responses to NaCN and dopamine. SNP (1-2 mg/kg i.v.) increased basal f (x), but reduced the NaCN-induced increases of f(x) over baseline and the transient f(x) inhibitions induced by dopamine, but not those prod uced by hyperoxia. Present results indicate that besides the known inh ibitory effect of NO on chemosensory responses to low PO2, NO also blo cks the chemosensory response to dopamine, leaving hyperoxic responses largely unchanged. (C) 1998 Elsevier Science B.V. All rights reserved .