Hypoxia elevates splanchnic sympathetic nerve activity (SNA) with differential effects during inspiration and expiration by unresolved central mechanisms. We examined the hypothesis that cardiovascular-related neurones in the caudal ventrolateral medulla (CVLM) contribute to the complex sympathetic response to
hypoxia. In
chloralose-anaesthetized, ventilated, vagotomized rats, acute
hypoxia (10% O2, 60 s) evoked an increase in SNA (103 +/- 12%) that was characterized by a decrease in activity during early inspiration followed by a prominent rise during expiration. Some recorded baro-activated CVLM neurones (n = 13) were activated by
hypoxia, and most of these neurones displayed peak activity during inspiration that was enhanced during
hypoxia. In contrast, other baro-activated CVLM neurones were inhibited during
hypoxia (n = 6), and most of these neurones showed peak activity during expiration prior to the onset of
hypoxia. Microinjection of the
glutamate antagonist kynurenate into the CVLM eliminated the respiratory-related fluctuations in SNA during
hypoxia and exaggerated the magnitude of the sympathetic response. In contrast, microinjection of a
GABA(A) antagonist (
bicuculline or
gabazine) into the CVLM dramatically attenuated the sympathetic response to
hypoxia. These data suggest the response to
hypoxia in baro-activated CVLM neurones is related to their basal pattern of respiratory-related activity, and changes in the activity of these neurones is consistent with a contribution to the respiratory-related sympathetic responses to
hypoxia. Furthermore, both
glutamate and
GABA in the CVLM contribute to the complex sympathetic response to acute
hypoxia.