Excitatory amino acid receptors in the rostral ventrolateral medulla mediate hypertension induced by carotid body chemoreceptor stimulation

1994 ◽  
Vol 349 (6) ◽  
pp. 549-554 ◽  
Author(s):  
M. Amano ◽  
T. Asari ◽  
T. Kubo
Keyword(s):  
Amino Acid ◽  
Carotid Body ◽  
Excitatory Amino Acid ◽  
Rostral Ventrolateral Medulla ◽  
Ventrolateral Medulla ◽  
Excitatory Amino Acid Receptors ◽  
Amino Acid Receptors

scholarly journals Is visceral sympathoexcitation to heat stress dependent on activation of ionotropic excitatory amino acid receptors in the rostral ventrolateral medulla?

2011 ◽  
Vol 301 (2) ◽  
pp. R548-R557 ◽  
Author(s):  
M. J. Kenney ◽  
C. N. Meyer ◽  
K. G. Hosking ◽  
R. J. Fels
Keyword(s):  
Heat Stress ◽  
Amino Acid ◽  
Excitatory Amino Acid ◽  
Rostral Ventrolateral Medulla ◽  
Ventrolateral Medulla ◽  
Inhibitory Input ◽  
Excitatory Amino Acid Receptors ◽  
Amino Acid Receptors ◽  
Young Rats ◽  
Stress Dependent

Acute heat stress activates visceral sympathetic nerve discharge (SND) in young rats, and the functional integrity of the rostral ventrolateral medulla (RVLM) is required for sustaining visceral sympathoexcitation during peak increases in internal body temperature (Tc). However, RVLM mechanisms mediating SND activation to hyperthermia remain unknown. In the present study, we investigated the role of RVLM ionotropic excitatory amino acid receptors in mediating visceral SND activation to heat stress in anesthetized, young rats. The effects of bilateral RVLM kynurenic acid (Kyn; 2.7 and 5.4 nmol), saline, or muscimol (400–800 pmol) microinjections on renal SND and splenic SND responses to heat stress were determined at peak hyperthermia (Tc 41.5°C), during progressive hyperthermia (Tc 40°C), and at the initiation of heating (Tc increased from 38 to 38.5°C). RVLM Kyn microinjections did not reduce renal and splenic SND recorded during progressive or peak hyperthermia and did not attenuate SND activation at the initiation of heating. In fact, renal and splenic SND tended to be or were significantly increased following RVLM Kyn microinjections at the initiation of heating and during hyperthermia (40 and 41.5°C). RVLM muscimol microinjections at 39, 40, and 41.5°C resulted in immediate reductions in SND. These data indicate that RVLM ionotropic glutamate receptors are required for mediating visceral sympathoexcitation to acute heating and suggest that acute heating activates an RVLM ionotropic excitatory amino acid receptor dependent inhibitory input, which reduces the level of visceral SND to heating.

Excitatory amino acid receptors in commissural nucleus of the NTS mediate carotid chemoreceptor responses

1993 ◽  
Vol 264 (1) ◽  
pp. R41-R50 ◽  
Author(s):  
A. Vardhan ◽  
A. Kachroo ◽  
H. N. Sapru
Keyword(s):  
Amino Acid ◽  
Carotid Body ◽  
Excitatory Amino Acid ◽  
Minute Ventilation ◽  
Neuronal Cell ◽  
Excitatory Amino Acid Receptors ◽  
Amino Acid Receptors ◽  
Neuronal Cell Bodies ◽  
Carotid Body Chemoreceptors ◽  
Stimulation Of

Stimulation of carotid body chemoreceptors by saline saturated with 100% CO2 elicited an increase in mean arterial pressure, respiratory rate, tidal volume, and minute ventilation (VE). Microinjections of L-glutamate into a midline area 0.5-0.75 mm caudal and 0.3-0.5 mm deep with respect to the calamus scriptorius increased VE. Histological examination showed that the site was located in the commissural nucleus of the nucleus tractus solitarii (NTS). The presence of excitatory amino acid receptors [N-methyl-D-aspartic acid (NMDA); kainate, quisqualate/alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA) and trans 1-amino-cyclopentane-trans-1,3-dicarboxylic acid (ACPD)] in this area was demonstrated by microinjections of appropriate agonists. Simultaneous blockade of NMDA and non-NMDA receptors by combined injections of DL-2-aminophosphonoheptanoate (AP-7; 1 nmol) and 6,7-dinitro-quinoxaline-2,3-dione (DNQX; 1 nmol) abolished the responses to stimulation of carotid body on either side. Combined injections of AP-7 and DNQX did not produce a nonspecific depression of neurons because the responses to another agonist, carbachol, remained unaltered. Inhibition of the neurons in the aforementioned area with microinjections of muscimol (which hyperpolarizes neuronal cell bodies but not fibers of passage) also abolished the responses to subsequent carotid body stimulation on either side.(ABSTRACT TRUNCATED AT 250 WORDS)

Role of excitatory amino acid receptors in cardiorespiratory coupling in ventrolateral medulla

1996 ◽  
Vol 271 (5) ◽  
pp. R1221-R1230 ◽  
Author(s):  
T. Miyawaki ◽  
J. Minson ◽  
L. Arnolda ◽  
J. Chalmers ◽  
I. Llewellyn-Smith ◽  
...  
Keyword(s):  
Amino Acid ◽  
Excitatory Amino Acid ◽  
Nmda Antagonist ◽  
Kainate Receptors ◽  
Ventrolateral Medulla ◽  
Respiratory Drive ◽  
Excitatory Amino Acid Receptors ◽  
Amino Acid Receptors ◽  
Somatosympathetic Responses

The role of (+/-)-alpha-amino-3-hydroxy-5-methyl-isoxazole-4-propionic acid (AMPA)-kainate and N-methyl-D-aspartate (NMDA) receptors in the rostral ventrolateral medulla (RVLM) and caudal ventrolateral medulla (CVLM) on the central respiratory drive (CRD)-related activity of splanchnic sympathetic nerve activity (SNA) was examined in rats. SNA increased during inspiration (I peak) and postinspiration (PI peak). Bilateral microinjections of 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX; AMPA-kainate antagonist) or DL-2-amino-5-phosphonovaleric acid (APV; NMDA antagonist) into RVLM abolished the PI, but not the I, peak. Blockade of all excitatory amino acid receptors in RVLM with kynurenate, or mixtures of APV and CNQX, also failed to eliminate the I peak. Somatosympathetic responses were abolished by CNQX injection into RVLM, but were unaffected by APV. CNQX, but not APV, injection into CVLM increased the PI peak of SNA. Our findings suggest the following. 1) Both NMDA and AMPA-kainate receptors in RVLM are involved in the coupling between the sympathetic nervous system and CRD, which generates the PI peak seen in SNA. 2) The I peak of SNA is independent of excitatory amino acid transmission within RVLM. 3) There are different relative amounts of NMDA and AMPA-kainate receptors at synapses where respiratory and somatic inputs converge onto RVLM neurons. 4) Glutamatergic inputs to CVLM neurons modulate the coupling between SNA and CRD in RVLM.

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