TONIC STIMULATION OF GABA(B) RECEPTORS IN THE NUCLEUS-TRACTUS-SOLITARIUS MODULATES THE BARORECEPTOR REFLEX

Previous studies have indicated that tonic stimulation of GABA(B) receptors in the nucleus tractus solitarius (NTS) contributes to the regulation of arterial blood pressure (AP). The present studies examined the hypotheses that (1) tonic stimulation of GABA(B) receptors in the NTS provides a tonic attenuation of the baroreceptor reflex and (2) enhanced stimulation of these GABA(B) receptors markedly attenuates the baroreceptor reflex resulting in an increase in AP. In chloralose-anesthetized rats electrical stimulation of the aortic depressor nerve elicited frequency-dependent decreases in AP and heart rate (HR). These responses were markedly attenuated, but not eliminated, by injection of the GABA(B) receptor agonist baclofen into the ipsilateral NTS. In contrast, the GABA(A) receptor agonist muscimol completely inhibited aortic depressor nerve-evoked responses. Blockade of GABA(B) receptors in the NTS by local injection of CGP-35348 elicited a dose-dependent decrease in AP, and a dose-dependent blockade of the pressor response elicited by injection of baclofen into the NTS. These results support the hypothesis that GABA acts tonically on GABA(B) receptors in the NTS to attenuate the baroreceptor reflex, thereby contributing to the regulation of AP.