Unilateral blockade of excitatory amino acid receptors in the nucleus tractus solitarii produces an inhibition of baroreflexes in rats.
Excitatory amino acid receptors and L-glutamate in the nucleus tractus solitarii (NTS) may be involved in the regulation of baroreceptor reflexes. To evaluate this hypothesis, we microinjected amino acid antagonists unilaterally into the rat NTS, and examined their effects on cardiovascular responses to electrical stimulation of the aortic nerve and on depressor responses to excitatory amino acid agonists microinjected into the NTS. Male Wistar rats were anesthesized with urethane, paralyzed, and artificially ventilated. Kynurenate (227 ng), an excitatory amino acid antagonist, injected ipsilaterally but not contralaterally into the NTS, markedly inhibited the depressor response to aortic nerve stimulation. L-Glutamate diethylester (GDEE, 3 micrograms), another excitatory amino acid antagonist, injected ipsilaterally into the NTS, also markedly inhibited both reflex depressor and bradycardic responses. MK-801 (30 ng), an N-methyl-D-aspartate (NMDA) receptor channel blocker, slightly inhibited the baroreflex responses, while Joro spider toxin JSTX-3 (17 ng), a glutamate receptor antagonist, did not affect them. Kynurenate (227 ng) and GDEE (3 micrograms) markedly inhibited the depressor response to the NMDA receptor agonist NMDA (0.3 ng), the quisqualate receptor agonist quisqualate (0.1 ng), the kainate receptor agonist kainate (0.1 ng), and L-glutamate (10 ng), microinjected into the NTS, while MK-801 (30 ng) reduced only the depressor response to NMDA (0.3 ng), and JSTX-3 (17 ng) reduced only the depressor response to kainate (0.1 ng). These findings provide evidence for the presence of excitatory amino acid receptors involved in mediating the aortic baroreceptor reflex in the rat NTS.(ABSTRACT TRUNCATED AT 250 WORDS)
Department of Pharmacology, Yokohama City University School of Medicine, Japan.
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D000818:Animals; D001011:Aorta / Q000294:innervation; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D004558:Electric Stimulation; D005971:Glutamates / Q000494:pharmacology; D018698:Glutamic Acid; D006339:Heart Rate / Q000187:drug effects / Q000502:physiology; D007608:Kainic Acid / Q000494:pharmacology; D007736:Kynurenic Acid / Q000494:pharmacology; D008297:Male; D009475:Neurons, Afferent / Q000187:drug effects* / Q000502:physiology; D011312:Pressure; D016318:Quisqualic Acid / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains; D017459:Receptors, Amino Acid; D011956:Receptors, Cell Surface / Q000037:antagonists & inhibitors*; D016194:Receptors, N-Methyl-D-Aspartate / Q000037:antagonists & inhibitors; D012018:Reflex / Q000187:drug effects* / Q000502:physiology
D005971:Glutamates; D017459:Receptors, Amino Acid; D011956:Receptors, Cell Surface; D016194:Receptors, N-Methyl-D-Aspartate; C011829:glutamic acid diethyl ester; D018698:Glutamic Acid; D016318:Quisqualic Acid; D007736:Kynurenic Acid; D007608:Kainic Acid