Cardiovascular responses elicited by gamma-aminobutyric acid in the nucleus tractus solitarius: evidence for action at the GABAB receptor.

Previous studies in this laboratory have shown that GABAergic neurotransmission in the nucleus tractus solitarius contributes to the maintenance of blood pressure. Increasing the synaptic action of GABA in the nucleus tractus solitarius by injection of the blocker of the uptake of GABA, nipecotic acid elevated blood pressure. The current studies examined the subtype of GABA receptor involved in mediating this response. Bilateral injections of (-)baclofen into the nucleus tractus solitarius (1-100 pmol in 100 nl) of chloralose-anesthetized, paralyzed, ventilated Sprague-Dawley rats increased blood pressure without significantly altering heart rate. This pressor response was neither attenuated nor blocked by the selective GABAA receptor antagonist bicuculline. Similarly, the pressor response elicited by the injection of nipecotic acid into the nucleus tractus solitarius was totally unaffected by the GABAA receptor blockade with bicuculline. Since nipecotic acid acts by potentiating the action of synaptic GABA, and the GABA present presumably can interact with both GABAA and GABAB receptors, the observation that bicuculline did not block or attenuate the pressor response to nipecotic acid suggests that the pressor response to the enhanced synaptic action of GABA in the nucleus tractus solitarius can be produced independently of the involvement of GABAA receptors, and presumably is mediated through an action on GABAB receptors.