Excitatory amino acids in rostral ventrolateral medulla support blood pressure during water deprivation in rats

2004 ◽  
Vol 286 (5) ◽  
pp. H1642-H1648 ◽  
Author(s):  
Virginia L. Brooks ◽  
Korrina L. Freeman ◽  
Kathy A. Clow
Keyword(s):  
Arterial Pressure ◽  
Sympathetic Activity ◽  
Excitatory Amino Acids ◽  
Water Deprivation ◽  
Excitatory Amino Acid ◽  
Plasma Osmolality ◽  
Rostral Ventrolateral Medulla ◽  
Ventrolateral Medulla ◽  
Strongly Correlated ◽  
Pressor Responses

Water deprivation is associated with regional increases in sympathetic tone, but whether this is mediated by changes in brain stem regulation of sympathetic activity is unknown. Therefore, this study tested the hypothesis that water deprivation increases excitatory amino acid (EAA) drive of the rostral ventrolateral medulla (RVLM), by determining whether bilateral microinjection of kynurenate (Kyn; 2.7 nmol) into the RVLM decreases arterial pressure more in water-deprived than water-replete rats. Plasma osmolality was increased in 48-h water-deprived rats (313 ± 1 mosmol/kgH2O; P < 0.05) compared with 24-h water-deprived rats (306 ± 2 mosmol/kgH2O) and water-replete animals (300 ± 2 mosmol/kgH2O). Kyn decreased arterial pressure by 28.1 ± 5.2 mmHg ( P < 0.01) in 48-h water-deprived rats but had no effect in water-replete rats (–5.9 ± 1.3 mmHg). Variable depressor effects were observed in 24-h water-deprived animals (–12.5 ± 2.4 mmHg, not significant); however, in all rats the Kyn depressor response was strongly correlated to the osmolality level ( P < 0.01; r2 = 0.47). The pressor responses to unilateral microinjection of increasing doses (0.1, 0.5, 1.0, and 5.0 nmol) of glutamate were enhanced ( P < 0.05) during water deprivation, but the pressor responses to intravenous phenylephrine injection were smaller ( P < 0.05). These data suggest that water deprivation increases EAA drive to the RVLM, in part by increasing responsiveness of the RVLM to EAA such as glutamate.

Acute and chronic increases in osmolality increase excitatory amino acid drive of the rostral ventrolateral medulla in rats

2004 ◽  
Vol 287 (6) ◽  
pp. R1359-R1368 ◽  
Author(s):  
Virginia L. Brooks ◽  
Korrina L. Freeman ◽  
Theresa L. O’Donaughy
Keyword(s):  
Amino Acid ◽  
Arterial Pressure ◽  
Blood Volume ◽  
Excitatory Amino Acid ◽  
Isotonic Saline ◽  
Plasma Osmolality ◽  
Saline Infusion ◽  
Ventrolateral Medulla ◽  
Depressor Response ◽  
Hypertonic Saline Infusion

Water deprivation is associated with increased excitatory amino acid (EAA) drive of the rostral ventrolateral medulla (RVLM), but the mechanism is unknown. This study tested the hypotheses that the increased EAA activity is mediated by decreased blood volume and/or increased osmolality. This was first tested in urethane-anesthetized rats by determining whether bilateral microinjection of kynurenate (KYN, 2.7 nmol) into the RVLM decreases arterial pressure less in water-deprived rats after normalization of blood volume by intravenous infusion of isotonic saline or after normalization of plasma osmolality by intravenous infusion of 5% dextrose in water (5DW). Water-deprived rats exhibited decreased plasma volume and elevated plasma osmolality, hematocrit, and plasma sodium, chloride, and protein levels (all P < 0.05). KYN microinjection decreased arterial pressure by 24 ± 2 mmHg ( P < 0.05; n = 17). The depressor response was not altered following isotonic saline infusion but, while still present ( P < 0.05), was reduced ( P < 0.05) to −13 ± 2 mmHg soon after 5DW infusion. These data suggest that the high osmolality, but not low blood volume, contributes to the KYN depressor response. To further investigate the action of increased osmolality on EAA input to RVLM, water-replete rats were also studied after hypertonic saline infusion. Whereas KYN microinjection did not decrease pressure immediately following the infusion, a depressor response gradually developed over the next 3 h. Lumbar sympathetic nerve activity also gradually increased to up to 167 ± 19% of control ( P < 0.05) 3 h after hypertonic saline infusion. In conclusion, acute and chronic increases in osmolality appear to increase EAA drive of the RVLM.

Spinal NMDA receptors mediate pressor responses evoked from the rostral ventrolateral medulla

1991 ◽  
Vol 260 (1) ◽  
pp. H267-H275 ◽  
Author(s):  
M. K. Bazil ◽  
F. J. Gordon
Keyword(s):  
Spinal Cord ◽  
Heart Rate ◽  
Nmda Receptors ◽  
Excitatory Amino Acid ◽  
Cardiovascular Responses ◽  
Rostral Ventrolateral Medulla ◽  
Ventrolateral Medulla ◽  
Thoracic Spinal Cord ◽  
Thoracic Spinal ◽  
Pressor Responses

These studies investigated the role of spinal N-methyl-D-aspartic acid (NMDA) receptors in the mediation of cardiovascular responses evoked by L-glutamate (L-Glu) stimulation of the rostral ventrolateral medulla (RVM). Microinjections of L-Glu into the RVM of urethan-anesthetized rats increased mean arterial pressure (MAP) and heart rate. Intrathecal administration of the NMDA receptor antagonists D-(-)-2-amino-7-phosphonoheptanoic acid (D-AP-7) or 3-((+-)-2-carboxypiperazin-4-yl)-propyl-1-phosphonate (CPP) reduced MAP and heart rate. Blockade of NMDA receptors by D-AP-7 or CPP in the caudal thoracic spinal cord markedly reduced RVM pressor responses with little effect on evoked tachycardia. Administration of D-AP-7 to the rostral thoracic spinal cord had no effect on RVM pressor or tachycardic responses. Intrathecal D-AP-7 and CPP abolished the cardiovascular effects of intrathecal NMDA without reducing those produced by intrathecal kainic acid or the quisqualate agonist DL-alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA). These results indicate that 1) tonic activation of spinal NMDA receptors participates in the maintenance of sympathetic outflow to the heart and blood vessels, 2) pressor responses evoked from the RVM require synaptic activation of spinal NMDA receptors, and 3) an excitatory amino acid may be the neurotransmitter of pressor pathways descending from the RVM to the spinal cord.

Dorsomedial medulla is more susceptible than rostral ventrolateral medulla to hypoxic insult in cats

2001 ◽  
Vol 90 (1) ◽  
pp. 248-260 ◽  
Author(s):  
Ling-Zong Hong ◽  
Jon-Son Kuo ◽  
Mao-Hsiung Yen ◽  
Chok-Yung Chai
Keyword(s):  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Systemic Arterial Pressure ◽  
Rostral Ventrolateral Medulla ◽  
Ventrolateral Medulla ◽  
Nerve Activity ◽  
Pressor Responses ◽  
Norepinephrine Depletion ◽  
Vertebral Nerve

We investigated the responses of systemic arterial pressure and vertebral sympathetic nerve activity to glutamate microinjections (0.1 M, 70 nl) in the dorsomedial (DM) and the rostral ventrolateral medulla (RVLM) before hypoxia and after reoxygenation (posthypoxia) after various degrees of hypoxia in anesthetized cats. Hypoxia was produced by ventilating 5% O2 and 95% N2 for different durations (hypoxia I-III). In intact cats, the glutamate-induced systemic arterial pressure and vertebral nerve activity responses of the DM were depressed after all degrees of hypoxia. Posthypoxic depression in the RVLM, however, was not observed until hypoxia II and III. Precollicular decerebration prevented depression in the RVLM, but, for the DM, it was effective only for hypoxia I. Baro- and chemoreceptor denervation abolished all posthypoxic depression in both the DM and the RVLM. Pressor responses to tyramine (100–400 μg/kg iv) remained unchanged after all degrees of hypoxia. These results suggest that the DM is more susceptible to hypoxia than the RVLM. The peripheral baro- and chemoreceptors and the suprapontine structures apparently play an important role in posthypoxic depression. Moreover, the depression is not due to the postganglionic norepinephrine depletion.

Role of rostral ventrolateral medulla in centrally mediated pressor responses

1994 ◽  
Vol 267 (4) ◽  
pp. H1549-H1556 ◽  
Author(s):  
J. M. Kiely ◽  
F. J. Gordon
Keyword(s):  
Synaptic Transmission ◽  
Excitatory Amino Acid ◽  
Receptor Activation ◽  
Rostral Ventrolateral Medulla ◽  
Ventrolateral Medulla ◽  
Synaptic Activation ◽  
Axonal Conduction ◽  
Pressor Responses ◽  
Stimulation Of

The region of the rostral ventrolateral medulla (RVLM) plays an important role in central nervous system regulation of cardiovascular function. The initial purpose of these studies was to determine whether synaptic activation of excitatory amino acid (EAA) receptors in the RVLM might mediate central pressor responses. Blockade of EAA receptors in the RVLM with kynurenic acid abolished pressor responses evoked by stimulation of sciatic nerve afferents but had no effect on increases in arterial pressure produced by stimulation of hypothalamic sites. To determine whether synaptic transmission in the RVLM, independent of EAA receptor activation, was a prerequisite for the production of hypothalamic pressor responses, axonal conduction and/or synaptic transmission were pharmacologically interrupted in the RVLM. Blockade of synaptic transmission with muscimol or kainic acid attenuated, but did not eliminate, hypothalamic pressor responses. Concurrent blockade of synaptic and axonal transmission in the RVLM with lidocaine produced the greatest reduction of hypothalamic pressor responses. Collectively, these results suggest that central pressor responses are not uniformly mediated by synaptic activation of neurons within the RVLM. Instead, a combination of synaptic transmission and axonal conduction within and possibly outside the region of the RVLM may be required for the production of many centrally mediated pressor responses.

Connections between the pontine reticular formation and rostral ventrolateral medulla

1993 ◽  
Vol 265 (4) ◽  
pp. H1386-H1392 ◽  
Author(s):  
A. V. Krassioukov ◽  
L. C. Weaver
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Reticular Formation ◽  
Excitatory Amino Acid ◽  
Sympathetic Nerves ◽  
Blocking Agent ◽  
Rostral Ventrolateral Medulla ◽  
Ventrolateral Medulla ◽  
Pontine Reticular Formation ◽  
Renal Nerve

Pontine reticular formation (PRF) neurons provide tonic excitatory drive to sympathetic nerves and are involved in cardiovascular control [K. Hayes and L. C. Weaver. Am. J. Physiol. 263 (Heart Circ. Physiol. 32): H1567-H1575, 1992]. However, connections between the PRF and the well-known vasomotor region in the rostral ventrolateral medulla (RVLM) are unknown. In propofol (Diprivan)- anesthetized rats we investigated arterial pressure, heart rate, and renal nerve responses to microinjection of glycine (1.0 M, 60 nl) into the PRF before and after injection of the synaptic blocking agent cobalt chloride (4.0 mM, 200 nl) into the RVLM. Glycine injections into the PRF caused decreases in arterial pressure, heart rate, and discharge of renal sympathetic nerves. Synaptic blockade of the RVLM almost eliminated cardiovascular and sympathetic responses to glycine injections into the PRF and blocked somatosympathetic reflexes in the renal nerve. Cobalt injections into the RVLM had very small effects on basal renal nerve firing, arterial pressure, or heart rate. These results suggest that the neurons within the RVLM relay influences from the PRF to sympathetic preganglionic neurons. Because injections of the excitatory amino acid antagonist, kynurenate, into the RVLM also interrupted responses to blockade of the PRF and blocked somatosympathetic reflexes, glutamate is a likely neurotransmitter from the PRF to the RVLM and for somatosympathetic reflexes.

Rostral ventrolateral medulla and sympathorespiratory integration in rats

1990 ◽  
Vol 259 (5) ◽  
pp. R1063-R1074 ◽  
Author(s):  
P. G. Guyenet ◽  
R. A. Darnall ◽  
T. A. Riley
Keyword(s):  
Arterial Pressure ◽  
Respiratory Rate ◽  
Receptor Antagonist ◽  
Gabab Receptor ◽  
Excitatory Amino Acid ◽  
Respiratory Rhythm ◽  
Rostral Ventrolateral Medulla ◽  
Ventrolateral Medulla ◽  
Respiratory Modulation ◽  
Nerve Discharge

The respiratory modulation of the lumbar sympathetic nerve discharge (LSND) was examined in halothane-anesthetized, paralyzed, and vagotomized rats by means of phrenic nerve discharge (PND)-triggered histograms. The respiratory modulation was 1) proportional to PND amplitude during chemoreceptor activation with CO2 and 2) reduced at elevated arterial pressure. Bilateral injections of bicuculline [gamma-aminobutyric acid (GABA)A receptor antagonist, n = 5] into the rostral ventrolateral medulla (RVLM), but not into medullary raphe, reversibly increased mean arterial pressure (MAP) and resting LSND, decreased the baroreflex, reduced PND amplitude and central respiratory rate, and greatly magnified the respiratory modulation of LSND. Injections of strychnine (glycine receptor antagonist, n = 5) or phaclofen (GABAB receptor antagonist, n = 2) into RVLM were without effect. Injections of kynurenic acid (excitatory amino acid receptor antagonist) into RVLM (n = 8), but not raphe (n = 3), reduced PND amplitude, increased central respiratory rate, reduced MAP, elevated resting LSND slightly, and greatly reduced the respiratory modulation of LSND. These data suggest that the rostral tip of the ventrolateral medulla represents a critical link between the central respiratory rhythm generator and the vasomotor outflow. Also, it indicates that the respiratory modulation of SND does not involve a gating of the activity of the medullary neurons that convey baroreceptor information to RVLM sympathoexcitatory neurons.

scholarly journals Blockade of Rostral Ventrolateral Medulla Apelin Receptors Does Not Attenuate Arterial Pressure in SHR and L-NAME-Induced Hypertensive Rats

2018 ◽  
Vol 9 ◽  
Author(s):  
Philip R. Griffiths ◽  
Stephen J. Lolait ◽  
Louise E. Pearce ◽  
Fiona D. McBryde ◽  
Julian F. R. Paton ◽  
...  
Keyword(s):  
Arterial Pressure ◽  
Rostral Ventrolateral Medulla ◽  
Ventrolateral Medulla ◽  
Hypertensive Rats

Cerebral metabolic responses and vasopressin and oxytocin secretions during progressive water deprivation in rats

1992 ◽  
Vol 262 (2) ◽  
pp. R310-R317 ◽  
Author(s):  
M. Kadekaro ◽  
J. Y. Summy-Long ◽  
S. Freeman ◽  
J. S. Harris ◽  
M. L. Terrell ◽  
...  
Keyword(s):  
Water Deprivation ◽  
Glucose Utilization ◽  
Extracellular Volume ◽  
Plasma Osmolality ◽  
Ventrolateral Medulla ◽  
Ang Ii ◽  
Neural Lobe ◽  
Arterial Blood ◽  
Organum Vasculosum Laminae Terminalis ◽  
Enhanced Secretion

Progressive water deprivation increased plasma osmolality, plasma Na+ concentration, and hematocrit in proportion to the severity of dehydration. With increases of 2% in plasma osmolality (24 h dehydration), glucose utilization increased in the supraoptic nuclei and tended to increase in the neural lobe. With further dehydration, glucose utilization also increased in the paraventricular nuclei. These increases were paralleled by depletion of vasopressin and oxytocin contents in the neural lobe and by the enhanced secretion of both hormones into plasma, with a predominant increase of vasopressin. These changes were proportional to the degree of dehydration. With progression of dehydration, decreases in intracellular and extracellular volumes accentuate. Reductions in extracellular volume result in increased angiotensin II (ANG II) formation. Accordingly, glucose utilization in the subfornical organ (SFO), a primary site of ANG II action, increased after 48 and 72 h of dehydration. The median preoptic nucleus, which receives direct inputs from the SFO, also increased glucose utilization at these times. Glucose utilization also increased in the organum vasculosum laminae terminalis, probably in response to the converging inputs from osmoreceptors, volume receptors, and ANG II receptors. Decreases in glucose utilization were observed in the caudal and rostral ventrolateral medulla, perhaps as compensatory responses to decreased extracellular volume to prevent fall in arterial blood pressure.

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