PMID- 23680118
OWN - NLM
STAT- MEDLINE
DCOM- 20140113
LR  - 20130612
IS  - 1879-0712 (Electronic)
IS  - 0014-2999 (Linking)
VI  - 713
IP  - 1-3
DP  - 2013 Aug 5
TI  - Involvement of N-methyl-D-aspartate glutamate receptor and nitric oxide in 
      cardiovascular responses to dynamic exercise in rats.
PG  - 16-24
LID - S0014-2999(13)00374-9 [pii]
LID - 10.1016/j.ejphar.2013.04.046 [doi]
AB  - Dynamic exercise evokes sustained cardiovascular responses, which are 
      characterized by arterial pressure and heart rate increases. Although it is well 
      accepted that there is central nervous system mediation of cardiovascular 
      adjustments during exercise, information on the role of neural pathways and 
      signaling mechanisms is limited. It has been reported that glutamate, by acting 
      on NMDA receptors, evokes the release of nitric oxide through activation of 
      neuronal nitric oxide synthase (nNOS) in the brain. In the present study, we 
      tested the hypothesis that NMDA receptors and nNOS are involved in cardiovascular 
      responses evoked by an acute bout of exercise on a rodent treadmill. Moreover, we 
      investigated possible central sites mediating control of responses to exercise 
      through the NMDA receptor-nitric oxide pathway. Intraperitoneal administration of 
      the selective NMDA glutamate receptor antagonist dizocilpine maleate (MK-801) 
      reduced both the arterial pressure and heart rate increase evoked by dynamic 
      exercise. Intraperitoneal treatment with the preferential nNOS inhibitor 
      7-nitroindazole reduced exercise-evoked tachycardiac response without affecting 
      the pressor response. Moreover, treadmill running increased NO formation in the 
      medial prefrontal cortex (MPFC), bed nucleus of the stria teminalis (BNST) and 
      periaqueductal gray (PAG), and this effect was inhibited by systemic pretreatment 
      with MK-801. Our findings demonstrate that NMDA receptors and nNOS mediate the 
      tachycardiac response to dynamic exercise, possibly through an NMDA receptor-NO 
      signaling mechanism. However, NMDA receptors, but not nNOS, mediate the 
      exercise-evoked pressor response. The present results also provide evidence that 
      MPFC, BNST and PAG may modulate physiological adjustments during dynamic exercise 
      through NMDA receptor-NO signaling.
CI  - Copyright (c) 2013 Elsevier B.V. All rights reserved.
FAU - Camargo, Laura H A
AU  - Camargo LH
AD  - Laboratory of Pharmacology, Department of Natural Active Principles and 
      Toxicology, School of Pharmaceutical Sciences, Sao Paulo State University, UNESP, 
      Araraquara, SP, 14801-902, Brazil.
FAU - Alves, Fernando H F
AU  - Alves FH
FAU - Biojone, Caroline
AU  - Biojone C
FAU - Correa, Fernando M A
AU  - Correa FM
FAU - Resstel, Leonardo B M
AU  - Resstel LB
FAU - Crestani, Carlos C
AU  - Crestani CC
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20130514
PL  - Netherlands
TA  - Eur J Pharmacol
JT  - European journal of pharmacology
JID - 1254354
RN  - 0 (Receptors, N-Methyl-D-Aspartate)
RN  - 31C4KY9ESH (Nitric Oxide)
RN  - 6LR8C1B66Q (Dizocilpine Maleate)
RN  - EC 1.14.13.39 (Nitric Oxide Synthase Type I)
RN  - EC 1.14.13.39 (Nos1 protein, rat)
SB  - IM
MH  - Animals
MH  - Arterial Pressure/drug effects
MH  - Brain/drug effects/*metabolism
MH  - *Cardiovascular Physiological Phenomena/drug effects
MH  - Dizocilpine Maleate/pharmacology
MH  - Heart Rate/drug effects
MH  - Kinetics
MH  - Male
MH  - Nitric Oxide/*metabolism
MH  - Nitric Oxide Synthase Type I/*metabolism
MH  - Physical Conditioning, Animal/*physiology
MH  - Rats
MH  - Rats, Wistar
MH  - Receptors, N-Methyl-D-Aspartate/antagonists & inhibitors/*metabolism
MH  - Signal Transduction
EDAT- 2013/05/18 06:00
MHDA- 2014/01/15 06:00
CRDT- 2013/05/18 06:00
PHST- 2012/10/26 00:00 [received]
PHST- 2013/04/24 00:00 [revised]
PHST- 2013/04/26 00:00 [accepted]
PHST- 2013/05/18 06:00 [entrez]
PHST- 2013/05/18 06:00 [pubmed]
PHST- 2014/01/15 06:00 [medline]
AID - S0014-2999(13)00374-9 [pii]
AID - 10.1016/j.ejphar.2013.04.046 [doi]
PST - ppublish
SO  - Eur J Pharmacol. 2013 Aug 5;713(1-3):16-24. doi: 10.1016/j.ejphar.2013.04.046. 
      Epub 2013 May 14.