Research article summary (published 29 Jun 2009):

Role of N-methyl-D-aspartate and non-N-methyl-D-aspartate receptors in the cardiovascular effects of L-glutamate microinjection into the hypothalamic paraventricular nucleus of unanesthetized rats.

Full Abstract

We report on the cardiovascular effects of L-glutamate (L-glu) microinjection into the hypothalamic paraventricular nucleus (PVN) as well as the mechanisms involved in their mediation. L-glu microinjection into the PVN caused dose-related pressor and tachycardiac responses in unanesthetized rats. These responses were blocked by intravenous (i.v.) pretreatment with the ganglion blocker pentolinium (PE; 5 mg/kg), suggesting sympathetic mediation. Responses to L-glu were not affected by local microinjection of the selective non-NMDA receptor antagonist NBQX (2 nmol) or by local microinjection of the selective NMDA receptor antagonist LY235959 (LY; 2 nmol). However, the tachycardiac response was changed to a bradycardiac response after treatment with LY235959, suggesting that NMDA receptors are involved in the L-glu heart rate response. Local pretreatment with LY235959 associated with systemic PE or dTyr(CH(2))(5)(Me)AVP (50 microg/kg) respectively potentiated or blocked the response to L-glu, suggesting that L-glu responses observed after LY235959 are vasopressin mediated. The increased pressor and bradycardiac responses observed after LY + PE was blocked by subsequent i.v. treatment with the V(1)-vasopressin receptor antagonist dTyr(CH(2))(5)(Me)AVP, suggesting vasopressin mediation. The pressor and bradycardiac response to L-glu microinjection into the PVN observed in animals pretreated with LY + PE was progressively inhibited and even blocked by additional pretreatment with increasing doses of NBQX (2, 10, and 20 nmol) microinjected into the PVN, suggesting its mediation by local non-NMDA receptors. In conclusion, results suggest the existence of two glutamatergic pressor pathways in the PVN: one sympathetic pathway that is mediated by NMDA receptors and a vasopressinergic pathway that is mediated by non-NMDA receptors. (c) 2009 Wiley-Liss, Inc.

Author information

Author/s: Busnardo, Cristiane (C); Tavares, Rodrigo F (RF); Corrêa, Fernando M A (FM);

Affiliation: Department of Pharmacology, School of Medicine of Ribeirão Preto, University of São Paulo, Ribeirão Preto, São Paulo, Brazil.

Journal and publication information

Publication Type: Journal Article; Research Support, Non-U.S. Gov't

Journal: Journal of neuroscience research (J Neurosci Res), published in United States. (Language: eng)

Reference: 2009-Jul; vol 87 (issue 9) : pp 2066-77

Dates: Created 2009/05/14; Completed 2009/08/14;

PMID: 19229989, status: MEDLINE (last retrieval date: 8/21/2009, IMS Date: )

Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.

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MeSH headings (categories)

This article was linked to the MESH Headings shown below.

Animals Arginine Vasopressin - analogs & derivatives; metabolism; pharmacology Autonomic Pathways - drug effects; metabolism Blood Pressure - drug effects; physiology Cardiovascular Physiological Phenomena - drug effects Dose-Response Relationship, Drug Excitatory Amino Acid Antagonists - pharmacology Ganglionic Blockers - pharmacology Glutamic Acid - metabolism; pharmacology

Heart Rate - drug effects; physiology Male Microinjections Neurons - drug effects; metabolism Paraventricular Hypothalamic Nucleus - drug effects; metabolism Rats Rats, Wistar Receptors, N-Methyl-D-Aspartate - drug effects; metabolism Sympathetic Nervous System - drug effects; metabolism

Associated Chemicals: Excitatory Amino Acid Antagonists (0) ; Ganglionic Blockers (0) ; Receptors, N-Methyl-D-Aspartate (0) ; Arginine Vasopressin (113-79-1) ; Glutamic Acid (56-86-0)

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