title: Bradycardic and hypotensive responses to microinjection of L-glutamate into the lateral aspect of the commissural NTS are blocked by an NMDA receptor antagonist.
abstract: Baroreflex activation by phenylephrine infusion produces a bradycardic response while microinjection of L-glutamate into the most lateral aspect of the commissural nucleus tractus solitarius (NTS, 0.8 mm lateral to the midline) produces bradycardic and hypotensive responses. In the present study we investigated the role of NMDA receptors in the lateral aspect of the commissural NTS (0.8 mm lateral to the midline) in the bradycardic and hypotensive responses to microinjection of L-glutamate as well as in the processing of the bradycardic response to the baroreflex activation. The hypotensive and bradycardic responses to L-glutamate microinjection into the NTS were blocked by methyl-atropine (intravenous, i.v.), indicating that the hypotensive response was secondary to the bradycardia. Microinjection of L-glutamate (1 nmol/50 nl) into the NTS was performed before and after microinjection of increasing doses of phosphonovaleric acid (AP-5, a selective NMDA antagonist) at the same site. The microinjection of AP-5 [0.5 (n = 9), 2.0 (n = 8) and 10.0 nmol/50 nl (n = 7)] into the NTS (0.8 mm lateral to the midline) produced a dose-dependent blockade of the bradycardic and hypotensive responses to L-glutamate. In a specific group of rats the microinjection of 10 nmol/50 nl of AP-5 produced a significant reduction in baroreflex sensitivity 2 min after microinjection into the lateral NTS [gain = -1.48 +/- 0.12 vs. -0.5 +/- 0.2 beats/mmHg, (n = 5)], which was reversible. The data show that the bradycardic responses produced by microinjection of L-glutamate into the most lateral aspect of the commissural NTS or by activation of the baroreflex were blocked by microinjection of AP-5, indicating that the neurotransmission of the parasympathetic component of the baroreflex in the neurons of the lateral aspect of the commissural NTS involves NMDA receptors.
authors.affiliation: Department of Physiology, School of Medicine of Ribeirão Preto, University of São Paulo, Brazil.
authors.forename: R O
authors.initials: RO
authors.lastname: Canesin
authors.forename: L G
authors.initials: LG
authors.lastname: Bonagamba
authors.forename: B H
authors.initials: BH
authors.lastname: Machado
mesh_terms: D015763:2-Amino-5-phosphonovalerate / Q000494:pharmacology*; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D001919:Bradycardia / Q000139:chemically induced*; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology*; D018698:Glutamic Acid / Q000008:administration & dosage / Q000494:pharmacology; D006339:Heart Rate / Q000187:drug effects; D007022:Hypotension / Q000139:chemically induced*; D008297:Male; D008845:Microinjections; D051381:Rats; D017208:Rats, Wistar; D016194:Receptors, N-Methyl-D-Aspartate / Q000037:antagonists & inhibitors*; D017552:Solitary Nucleus / Q000502:physiology*
chemical_list: D018691:Excitatory Amino Acid Antagonists; D016194:Receptors, N-Methyl-D-Aspartate; D018698:Glutamic Acid; D015763:2-Amino-5-phosphonovalerate