Spinal GABA(A) receptors do not mediate the sympathetic baroreceptor reflex in the rat

Activation of baroreceptors causes efferent sympathetic nerve activity (SNA ) to fall. Two mechanisms could account for this sympathoinhibition: disfac ilitation of sympathetic preganglionic neurons (SPN) and/or direct inhibiti on of SPN. The roles that spinal GABA and glycine receptors play in the bar oreceptor reflex were examined in anesthetized, paralyzed, and artificially ventilated rats. Spinal GABA(A) receptors were blocked by an intrathecal i njection of bicuculline methiodide, whereas glycine receptors were blocked with strychnine. Baroreceptors were activated by stimulation of the aortic depressor nerve (ADN), and a somatosympathetic reflex was used as control. After an intrathecal injection of vehicle, there was no effect on any measu red variable or evoked reflex. In contrast, bicuculline caused a dose-depen dent increase in arterial pressure, SNA, phrenic nerve discharge, and it si gnificantly facilitated the somatosympathetic reflex. However, bicuculline did not attenuate either the depressor response or sympathoinhibition evoke d after ADN stimulation. Similarly, strychnine did not affect the barorecep tor-induced depressor response. Thus GABA(A) and glycine receptors in the s pinal cord have no significant role in baroreceptor-mediated sympathoinhibi tion.