title: Modulation of the sympathetic response to acute hypoxia by the caudal ventrolateral medulla in rats.
abstract: 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.
authors.affiliation: Department of Physiology, Medical College of Georgia, Augusta, GA 30912-3000, USA.
authors.forename: Daniel A
authors.initials: DA
authors.lastname: Mandel
authors.forename: Ann M
authors.initials: AM
authors.lastname: Schreihofer
mesh_terms: D000818:Animals; D001640:Bicuculline / Q000494:pharmacology; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D018755:GABA Agonists / Q000494:pharmacology; D058787:GABA-A Receptor Antagonists; D018698:Glutamic Acid / Q000494:pharmacology; D000860:Hypoxia / Q000503:physiopathology*; D007736:Kynurenic Acid / Q000494:pharmacology; D008297:Male; D008526:Medulla Oblongata / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D008959:Models, Neurological; D009118:Muscimol / Q000494:pharmacology; D009474:Neurons / Q000187:drug effects / Q000502:physiology; D010791:Phrenic Nerve / Q000187:drug effects / Q000502:physiology; D011724:Pyridazines / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D018009:Receptors, Glycine / Q000037:antagonists & inhibitors; D015656:Respiratory Mechanics / Q000187:drug effects / Q000502:physiology; D012966:Sodium Cyanide / Q000494:pharmacology; D013153:Splanchnic Nerves / Q000187:drug effects / Q000502:physiology; D013331:Strychnine / Q000494:pharmacology; D013564:Sympathetic Nervous System / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D014628:Vagotomy
chemical_list: D018691:Excitatory Amino Acid Antagonists; D018755:GABA Agonists; D058787:GABA-A Receptor Antagonists; D011724:Pyridazines; D018009:Receptors, Glycine; D009118:Muscimol; D018698:Glutamic Acid; C049853:gabazine; D007736:Kynurenic Acid; D013331:Strychnine; D012966:Sodium Cyanide; D001640:Bicuculline