N-methyl-D-aspartate receptors in the insular cortex modulate baroreflex in unanesthetized rats.
In the present study, we report the effect of insular cortex (IC) ablation caused by bilateral microinjection of the non-selective synaptic blocker CoCl(2) on cardiac baroreflex response in unanesthetized rats as well as the involvement of local glutamatergic neurotransmission. Unilateral (left or right) microinjection of CoCl(2) (1 nmol/ 100 nL) did not affect the bradycardiac response to blood pressure increase evoked by intravenous infusion of phenylephrine nor the tachycardiac response to blood pressure decrease caused by intravenous infusion of sodium nitroprusside, 10 min after CoCl(2). Bilateral microinjection of CoCl(2) into IC decreased the magnitude of reflex bradycardia without affecting tachycardiac responses. Baroreflex activity returned to control values 60 min after CoCl(2) microinjection, confirming its reversible effect. Further we studied the possible involvement of IC-glutamatergic neurotransmission in baroreflex modulation. We observed that bilateral microinjection of the selective NMDA receptor antagonist LY235959 (4 nmol/100 nL) into the IC decreased the magnitude of reflex bradycardia without affecting tachycardiac responses. IC treatment with the selective non-NMDA antagonist NBQX (4 nmol/100 nL) did not affect baroreflex activity. The results suggest that synapses within the IC have a tonic excitatory influence on the baroreflex parasympathetic component. Moreover, the present data suggest that local NMDA-receptors are involved in the IC-mediated tonic excitatory influence on baroreflex parasympathetic activity.
Alves
Fernando H F
FH
Department of Pharmacology, School of Medicine of Ribeirão Preto, University of São Paulo, Ribeirão Preto, SP, 14090-900, Brazil.
Crestani
Carlos C
CC
Resstel
Leonardo B M
LB
Correa
Fernando M A
FM
D000777:Anesthetics / Q000494:pharmacology; D000818:Animals; D000959:Antihypertensive Agents / Q000494:pharmacology; D017776:Autonomic Pathways / Q000033:anatomy & histology / Q000187:drug effects / Q000378:metabolism*; D017704:Baroreflex / Q000187:drug effects / Q000502:physiology*; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D001919:Bradycardia / Q000139:chemically induced; D002540:Cerebral Cortex / Q000033:anatomy & histology / Q000187:drug effects / Q000378:metabolism*; D003035:Cobalt / Q000494:pharmacology; D004525:Efferent Pathways / Q000033:anatomy & histology / Q000187:drug effects / Q000378:metabolism; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D018698:Glutamic Acid / Q000378:metabolism*; D006339:Heart Rate / Q000187:drug effects / Q000502:physiology; D007546:Isoquinolines / Q000494:pharmacology; D009474:Neurons / Q000187:drug effects / Q000378:metabolism; D009599:Nitroprusside / Q000494:pharmacology; D011810:Quinoxalines / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D016194:Receptors, N-Methyl-D-Aspartate / Q000819:agonists / Q000378:metabolism*; D009435:Synaptic Transmission / Q000187:drug effects / Q000502:physiology
D000777:Anesthetics; D000959:Antihypertensive Agents; D018691:Excitatory Amino Acid Antagonists; D007546:Isoquinolines; D011810:Quinoxalines; D016194:Receptors, N-Methyl-D-Aspartate; C062865:2,3-dioxo-6-nitro-7-sulfamoylbenzo(f)quinoxaline; D009599:Nitroprusside; D003035:Cobalt; D018698:Glutamic Acid; C088643:LY 235959; C018021:cobaltous chloride