PMID- 26861418
OWN - NLM
STAT- MEDLINE
DCOM- 20161213
LR  - 20161230
IS  - 1873-7544 (Electronic)
IS  - 0306-4522 (Linking)
VI  - 320
DP  - 2016 Apr 21
TI  - NMDA and non-NMDA glutamate receptors in the paraventricular nucleus of the 
      hypothalamus modulate different stages of hemorrhage-evoked cardiovascular 
      responses in rats.
PG  - 149-59
LID - S0306-4522(16)00118-4 [pii]
LID - 10.1016/j.neuroscience.2016.02.003 [doi]
AB  - Here we report the involvement of N-Methyl-d-Aspartate (NMDA) and non-NMDA 
      glutamate receptors from the paraventricular nucleus of the hypothalamus (PVN) in 
      the mediation of cardiovascular changes observed during hemorrhage and 
      post-bleeding periods. In addition, the present study provides further evidence 
      of the involvement of circulating vasopressin and cardiac sympathetic activity in 
      cardiovascular responses to hemorrhage. Systemic treatment with the 
      V1-vasopressin receptor antagonist dTyr(CH2)5(Me)AVP (50 mug/kg, i.v.) increased 
      the latency to the onset of hypotension during hemorrhage and slowed 
      post-bleeding recovery of blood pressure. Systemic treatment with the 
      beta1-adrenergic receptor antagonist atenolol (1 mg/kg, i.v.) also increased the 
      latency to the onset of hypotension during hemorrhage. Moreover, atenolol 
      reversed the hemorrhage-induced tachycardia into bradycardia. Bilateral 
      microinjection of the selective NMDA glutamate receptor antagonist LY235959 (2 
      nmol/100 nL) into the PVN blocked the hypotensive response to hemorrhage and 
      reduced the tachycardia during the post-hemorrhage period. Systemic treatment 
      with dTyr(CH2)5(Me)AVP inhibited the effect of LY235959 on hemorrhage-induced 
      hypotension, without affecting the post-bleeding tachycardia. PVN treatment with 
      the selective non-NMDA receptor antagonist NBQX (2 nmol/100 nL) reduced the 
      recovery of blood pressure to normal levels in the post-bleeding phase and 
      reduced hemorrhage-induced tachycardia. Combined blockade of both NMDA and 
      non-NMDA glutamate receptors in the PVN completely abolished the hypotensive 
      response in the hemorrhage period and reduced the tachycardiac response in the 
      post-hemorrhage period. These results indicate that local PVN glutamate 
      neurotransmission is involved in the neural pathway mediating cardiovascular 
      responses to hemorrhage, via an integrated control involving autonomic nervous 
      system activity and vasopressin release into the circulation.
CI  - Copyright (c) 2016 IBRO. Published by Elsevier Ltd. All rights reserved.
FAU - Busnardo, C
AU  - Busnardo C
AD  - Department of Pharmacology, School of Medicine of Ribeirao Preto, University of 
      Sao Paulo, Ribeirao Preto, Sao Paulo, Brazil. Electronic address: crisbus@usp.br.
FAU - Crestani, C C
AU  - Crestani CC
AD  - School of Pharmaceutical Sciences, Univ. Estadual Paulista-UNESP, Araraquara, SP, 
      Brazil.
FAU - Fassini, A
AU  - Fassini A
AD  - Department of Pharmacology, School of Medicine of Ribeirao Preto, University of 
      Sao Paulo, Ribeirao Preto, Sao Paulo, Brazil.
FAU - Resstel, L B M
AU  - Resstel LB
AD  - Department of Pharmacology, School of Medicine of Ribeirao Preto, University of 
      Sao Paulo, Ribeirao Preto, Sao Paulo, Brazil.
FAU - Correa, F M A
AU  - Correa FM
AD  - Department of Pharmacology, School of Medicine of Ribeirao Preto, University of 
      Sao Paulo, Ribeirao Preto, Sao Paulo, Brazil.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20160206
PL  - United States
TA  - Neuroscience
JT  - Neuroscience
JID - 7605074
RN  - 0 (Receptors, Glutamate)
SB  - IM
MH  - Animals
MH  - Cardiovascular System/*physiopathology
MH  - Disease Models, Animal
MH  - Hemodynamics/*physiology
MH  - Hemorrhage/*complications
MH  - Male
MH  - Paraventricular Hypothalamic Nucleus/*metabolism
MH  - Rats
MH  - Rats, Wistar
MH  - Receptors, Glutamate/*metabolism
OTO - NOTNLM
OT  - cardiovascular system
OT  - glutamate neurotransmission
OT  - hemorrhagic shock
OT  - paraventricular nucleus of hypothalamus
OT  - sympathetic activity
OT  - vasopressin
EDAT- 2016/02/11 06:00
MHDA- 2016/12/15 06:00
CRDT- 2016/02/11 06:00
PHST- 2015/10/19 00:00 [received]
PHST- 2016/01/18 00:00 [revised]
PHST- 2016/02/01 00:00 [accepted]
PHST- 2016/02/11 06:00 [entrez]
PHST- 2016/02/11 06:00 [pubmed]
PHST- 2016/12/15 06:00 [medline]
AID - S0306-4522(16)00118-4 [pii]
AID - 10.1016/j.neuroscience.2016.02.003 [doi]
PST - ppublish
SO  - Neuroscience. 2016 Apr 21;320:149-59. doi: 10.1016/j.neuroscience.2016.02.003. 
      Epub 2016 Feb 6.