Lack of involvement of GABA in baroreceptor-mediated sympathoinhibition.
The purpose of the present investigation was to determine if gamma-aminobutyric acid (GABA) mediates the baroreceptor-induced inhibition of sympathetic nerve discharge (SND) in dialurethan-anesthetized cats. The GABA antagonists picrotoxin and bicuculline produced marked elevations in arterial blood pressure and inferior cardiac SND. The inhibition of SND observed during pressor responses was occasionally slightly depressed after picrotoxin or bicuculline. Midcollicullar transection blocked or reversed the increase in blood pressure and SND produced by GABA antagonists. Under these conditions, baroreceptor inhibition of SND was not affected by picrotoxin. Microinjections of picrotoxin into the rostral ventrolateral medulla produced increases in arterial blood pressure and SND but failed to affect baroreceptor-induced sympathoinhibition. GABA antagonists given intravenously also failed to affect the baroreceptor-induced inhibition of sympathetically related neurons recorded in the rostral ventrolateral medulla. However, intravenous picrotoxin did antagonize the inhibitory affect of microiontophoretically applied GABA on these neurons. These data provide no evidence to support the contention that GABA mediates the baroreceptor-induced inhibition of SND. The role of GABA in regulating SND is discussed.
D000818:Animals; D002415:Cats; D004594:Electrophysiology; D006329:Heart Conduction System / Q000502:physiology; D008526:Medulla Oblongata / Q000502:physiology; D009433:Neural Inhibition; D009474:Neurons / Q000502:physiology; D011311:Pressoreceptors / Q000502:physiology*; D012018:Reflex / Q000502:physiology; D013564:Sympathetic Nervous System / Q000166:cytology / Q000502:physiology*; D005680:gamma-Aminobutyric Acid / Q000502:physiology*
D005680:gamma-Aminobutyric Acid