Sympathoexcitatory CVLM neurons mediate responses to caudal pressor area stimulation

2000 ◽  
Vol 279 (2) ◽  
pp. R364-R374 ◽  
Author(s):  
Madhusudan Natarajan ◽  
Shaun F. Morrison
Keyword(s):  
Arterial Pressure ◽  
Kynurenic Acid ◽  
Sympathetic Nerve Activity ◽  
Pressor Response ◽  
Ventrolateral Medulla ◽  
Homocysteic Acid ◽  
Premotor Neurons ◽  
Caudal Pressor ◽  
Excitatory Responses ◽  
Stimulation Of

Neurons in the caudal pressor area (CPA) are a source of tonic sympathoexcitation that is dependent on activation of cardiovascular sympathetic premotor neurons in the rostral ventrolateral medulla (RVLM). In the present study, we sought to clarify the mechanism through which CPA neurons elicit increases in RVLM neuronal discharge, vasoconstrictor sympathetic tone, and arterial pressure. In urethan-chloralose-anesthetized, paralyzed, and artificially ventilated rats, bilateral disinhibition of CPA with bicuculline (Bic) after bilateral disinhibition of caudal ventrolateral medulla (CVLM) caused increases in splanchnic sympathetic nerve activity (+277% control) and arterial pressure (+54 mmHg). Inhibition of CVLM neurons with muscimol abolished the pressor response to activation of CPA neurons, suggesting that neurons within CVLM mediate the excitatory responses from CPA. Disinhibition of CVLM and CPA with Bic enhanced the sympathoexcitatory responses to stimulation of CPA with dl-homocysteic acid, which were blocked by microinjections of kynurenic acid into CVLM. We conclude that the pathway from CPA to RVLM involves an obligatory glutamatergic activation of sympathoexcitatory neurons in the vicinity of CVLM.

Mechanisms of pressor response produced by stimulation of nucleus ambiguus

1990 ◽  
Vol 259 (5) ◽  
pp. R955-R962
Author(s):  
B. H. Machado ◽  
M. J. Brody
Keyword(s):  
Arterial Pressure ◽  
Vascular Resistance ◽  
Pressor Response ◽  
Nucleus Ambiguus ◽  
Ventrolateral Medulla ◽  
Pressor Responses ◽  
Regional Vascular Resistance ◽  
Parasympathetic Control ◽  
Renal Vascular ◽  
Stimulation Of

We showed previously that activation of nucleus ambiguus (NA) induced bradycardia and increased arterial pressure. In this study, we compared responses produced by electrical and chemical (glutamate) stimulation of NA and adjacent rostral ventrolateral medulla (RVLM). Equivalent pressor responses were elicited from both areas. However: 1) The response from RVLM was elicited at a lower frequency. 2) Regional vascular resistance changes were different, i.e., electrical stimulation of NA increased vascular resistance in hindquarters much more than the renal and mesenteric beds. In contrast, electrical and chemical stimulation of RVLM produced a more prominent effect on the renal vascular bed. 3) Bradycardia was elicited from NA at lower current intensity. 4) Glutamate produced bradycardia only when injected into NA. Studies in rats with sinoaortic deafferentation showed that bradycardic response to activation of NA was only partly reflex in origin. We conclude that 1) NA and RVLM control sympathetic outflow to regional vascular beds differentially and 2) the NA region involves parasympathetic control of heart rate and sympathetic control of arterial pressure.

Inhibition of rostral VLM by baroreceptor activation is relayed through caudal VLM

1990 ◽  
Vol 258 (5) ◽  
pp. R1271-R1278 ◽  
Author(s):  
S. K. Agarwal ◽  
A. J. Gelsema ◽  
F. R. Calaresu
Keyword(s):  
Kynurenic Acid ◽  
Cardiac Cycle ◽  
Pressor Response ◽  
Inhibitory Response ◽  
Firing Frequency ◽  
Ventrolateral Medulla ◽  
Cardiovascular Neurons ◽  
Baroreceptor Activation ◽  
Acid Administration ◽  
Stimulation Of

Experiments were done to test the hypothesis that inhibition of neurons in the rostral ventrolateral medulla (RVLM) elicited by stimulation of the nucleus tractus solitarii (NTS) is relayed through the caudal ventrolateral medulla (CVLM). We recorded activity from 56 spontaneously firing units in the right RVLM of urethan-anesthetized and artificially ventilated rats. Eleven of these units were classified as cardiovascular neurons, because they were silenced by baroreceptor activation (1-3 micrograms phenylephrine iv) and showed rhythmicity of their spontaneous activity in synchrony with the cardiac cycle. Single pulses (0.1 ms, 30-75 microA) delivered 1/s to depressor sites in the ipsilateral NTS inhibited the activity of all these cardiovascular neurons. Microinjection of the glutamate antagonist kynurenic acid (0.15 M, 50 nl) into the ipsilateral CVLM blocked the inhibitory response of RVLM units to the administration of phenylephrine and increased the firing frequency of cardiovascular neurons in the RVLM by 43%. Moreover, kynurenic acid administration attenuated the inhibitory response of cardiovascular neurons in the RVLM to NTS stimulation. Finally, stimulation of the NTS that elicited depressor responses under control conditions produced a pressor response after kynurenic acid administration. The remaining 45 RVLM neurons were barosensitive but lacked cardiac cycle-related rhythmicity. These results provide direct evidence for the existence of a tonic inhibitory pathway from NTS to RVLM that is relayed through the CVLM probably by a glutamatergic projection from NTS to CVLM.

scholarly journals Pregnancy and the endocrine regulation of the baroreceptor reflex

2010 ◽  
Vol 299 (2) ◽  
pp. R439-R451 ◽  
Author(s):  
Virginia L. Brooks ◽  
Roger A. L. Dampney ◽  
Cheryl M. Heesch
Keyword(s):  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Baroreceptor Reflex ◽  
Ventrolateral Medulla ◽  
Endocrine Regulation ◽  
Nerve Activity ◽  
Baroreflex Function ◽  
Premotor Neurons ◽  
The Brain

The purpose of this review is to delineate the general features of endocrine regulation of the baroreceptor reflex, as well as specific contributions during pregnancy. In contrast to the programmed changes in baroreflex function that occur in situations initiated by central command (e.g., exercise or stress), the complex endocrine milieu often associated with physiological and pathophysiological states can influence the central baroreflex neuronal circuitry via multiple sites and mechanisms, thereby producing varied changes in baroreflex function. During pregnancy, baroreflex gain is markedly attenuated, and at least two hormonal mechanisms contribute, each at different brain sites: increased levels of the neurosteroid 3α-hydroxy-dihydroprogesterone (3α-OH-DHP), acting in the rostral ventrolateral medulla (RVLM), and reduced actions of insulin in the forebrain. 3α-OH-DHP appears to potentiate baroreflex-independent GABAergic inhibition of premotor neurons in the RVLM, which decreases the range of sympathetic nerve activity that can be elicited by changes in arterial pressure. In contrast, reductions in the levels or actions of insulin in the brain blunt baroreflex efferent responses to increments or decrements in arterial pressure. Although plasma levels of angiotensin II are increased in pregnancy, this is not responsible for the reduction in baroreflex gain, although it may contribute to the increased level of sympathetic nerve activity in this condition. How these different hormonal effects are integrated within the brain, as well as possible interactions with additional potential neuromodulators that influence baroreflex function during pregnancy and other physiological and pathophysiological states, remains to be clearly delineated.

Ventrolateral medullary neurons modulate pressor reflex to muscular contraction

1989 ◽  
Vol 257 (5) ◽  
pp. R1154-R1161 ◽  
Author(s):  
R. M. Bauer ◽  
G. A. Iwamoto ◽  
T. G. Waldrop
Keyword(s):  
Arterial Pressure ◽  
Excitatory Amino Acid ◽  
Pressor Response ◽  
Minute Ventilation ◽  
Muscular Contraction ◽  
Posterior Hypothalamus ◽  
Ventrolateral Medulla ◽  
Pressor Reflex ◽  
Stimulation Of

Cardiorespiratory alterations during exercise are mediated through feedback from contracting muscles and descending drive from rostral brain sites such as the posterior hypothalamus. The role of medullary sites, which process this information, was examined in this study. In anesthetized cats, muscular contraction elicited by stimulation of L7 and S1 ventral roots and electrical stimulation of sites in the posterior hypothalamus both evoked increases in arterial pressure, heart rate, and minute ventilation. The reflex increase in arterial pressure produced by muscular contraction was attenuated significantly 15-20 min after bilateral microinjections of an excitatory amino acid (EAA) receptor antagonist, kynurenic acid (KYN), into the ventrolateral medulla (VLM). The reflex increase in arterial pressure evoked by muscular contraction returned to control levels 90 min after VLM microinjections of KYN. Microinjection of KYN into the VLM had no effect on the cardiorespiratory responses to posterior hypothalamic stimulation. These findings suggest that neurons in the VLM modulate the reflex pressor response evoked by muscular contraction. This reflex may be mediated through an interaction with EAA receptors on neurons in the VLM.

Blockade of glutamate receptors in CVLM and NTS attenuates airway dilation evoked from parabrachial region

1996 ◽  
Vol 81 (1) ◽  
pp. 400-407 ◽  
Author(s):  
A. M. Motekaitis ◽  
I. C. Solomon ◽  
M. P. Kaufman
Keyword(s):  
Glutamate Receptors ◽  
Kynurenic Acid ◽  
Cobalt Chloride ◽  
Nucleus Tractus Solitarii ◽  
Ventrolateral Medulla ◽  
Homocysteic Acid ◽  
Caudal Ventrolateral Medulla ◽  
Airway Response ◽  
Parabrachial Nuclei ◽  
Stimulation Of

Previous work from our laboratory has shown that stimulation of cell bodies and dendrites in the medial and lateral parabrachial nuclei dilates the airways. The sites participating in the pathway mediating this airway response are not known. Two likely candidates are the caudal ventrolateral medulla (CVLM) and the nucleus tractus solitarii (NTS). Using chloralose-anesthetized cats, we assessed the airway dilation evoked from the parabrachial region before and during bilateral blockade of the NTS or the CVLM. The airway dilation arising from stimulation of the parabrachial region was evoked by microinjection of DL-homocysteic acid (25 nl, 100 mM). Bilateral blockade of the NTS or CVLM, achieved by microinjection of kynurenic acid (50 nl, 100 mM), reversibly attenuated the airway dilation in every cat tested. On average, kynurenic acid-induced blockade of the NTS caused a more complete attenuation of the dilation evoked from the parabrachial region than did blockade of the CVLM. Bilateral microinjection of cobalt chloride (50 nl, 50 mM) into the CVLM gave inconclusive results, attenuating the airway dilation evoked from the parabrachial region in six cats and potentiating it in three others. We conclude that the CVLM and the NTS participate in the airway dilation arising from the parabrachial region.

Differential control of renal and splenic nerves without medullary topography

1991 ◽  
Vol 260 (4) ◽  
pp. H1072-H1079 ◽  
Author(s):  
D. J. Beluli ◽  
L. C. Weaver
Keyword(s):  
Spatial Organization ◽  
Excitatory Amino Acid ◽  
Sympathetic Nerves ◽  
Ventrolateral Medulla ◽  
Renal Nerve ◽  
Homocysteic Acid ◽  
Fixed Proportion ◽  
Excitatory Responses ◽  
Differential Control ◽  
Neuronal Groups

A previous study in our laboratory showed that pharmacological blockade of neurons in the rostral ventrolateral medulla has greater influence on the electrical activity of renal than splenic nerves (K. Hayes and L. C. Weaver, J. Physiol. Lond. 428: 371-385, 1990). This differential control of sympathetic nerves innervating different organs may be due to viscerotopic representation of the kidney and spleen within medullary neurons that control the vasculature. To search for this topographical organization, 15 nl (2.5 nmol) of the excitatory amino acid DL-homocysteic acid (DLH) was microinjected into the ventrolateral medulla (VLM) of rats anesthetized with urethan. No distinct viscerotopic organization was found in the rostral or caudal VLM. However, renal nerve responses were consistently greater than splenic by a fixed proportion. In summary, stimulation of rostral and caudal VLM neurons causes differential renal and splenic excitatory responses, but mechanisms providing this selective control do not involve spatial organization of neuronal groups in the VLM.

Activation of neurons in the rostral ventrolateral medulla increases bronchomotor tone in dogs

1991 ◽  
Vol 71 (1) ◽  
pp. 210-216 ◽  
Author(s):  
J. R. Haselton ◽  
P. A. Padrid ◽  
M. P. Kaufman
Keyword(s):  
Smooth Muscle ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Ventrolateral Medulla ◽  
Adrenergic Blockade ◽  
Homocysteic Acid ◽  
Lung Resistance ◽  
Anesthetized Dogs ◽  
Total Lung Resistance ◽  
Bronchomotor Tone

Previous work from this laboratory has demonstrated that the chemical activation of cell bodies in the caudal ventrolateral medulla of chloralose-anesthetized dogs decreased bronchomotor tone by withdrawing cholinergic input to airway smooth muscle. In the present study we determined the bronchomotor responses to microinjection of DL-homocysteic acid (100 mM; 25–50 nl) into the rostral ventrolateral (RVL) medulla of chloralose-anesthetized dogs. Total lung resistance was used as a functional index of bronchomotor tone. Microinjection of DL-homocysteic acid into the 20 sites located in the lateral aspect of the RVL medulla increased both total lung resistance [from 6.5 +/- 0.4 to 9.1 +/- 0.8 (SE) cmH2O.l-1.s; P less than 0.05] and mean arterial pressure (from 125 +/- 5 to 148 +/- 8 mmHg; P less than 0.05). Microinjection of this amino acid into nine sites located in the medial aspect of the RVL medulla increased mean arterial pressure (from 130 +/- 6 to 153 +/- 6 mmHg; P less than 0.05) but had no effect on total lung resistance. We confirmed in three sites that the increase in total lung resistance evoked by microinjection of DL-homocysteic acid was accompanied by an increase in tracheal smooth muscle tension. The increase in total lung resistance evoked by DL-homocysteic acid was not affected by beta-adrenergic blockade but was abolished by muscarinic blockade.

Effects of hypoxia, hyperoxia and hypercapnia on graded cerebral ischemic responses in rabbits

1992 ◽  
Vol 263 (6) ◽  
pp. H1839-H1846
Author(s):  
T. Takeuchi ◽  
J. Horiuchi ◽  
N. Terada ◽  
M. Nagao ◽  
H. Terajima
Keyword(s):  
Blood Flow ◽  
Cerebral Ischemia ◽  
Arterial Pressure ◽  
Internal Carotid ◽  
Pressor Response ◽  
Ventrolateral Medulla ◽  
Left Internal Carotid Artery ◽  
Renal Nerve ◽  
Tissue Po2 ◽  
Cerebral Ischemic

This study was designed to determine how several factors interact to modify the cerebral ischemic pressor response (CIR) in anesthetized rabbits. After the carotid sinus and aortic nerves were bilaterally sectioned, blood flow through the left internal carotid artery (ICF), which was surgically restricted as the sole route of blood supply to the brain, was reduced by a servo-controller during ventilation with room air, and 8% and 90% O2 and 2 and 5% CO2 gas mixtures. Blood flow (MBF), tissue PO2, PCO2, and interstitial pH were measured in the rostral ventrolateral medulla. Internal carotid arterial pressure, tissue PO2, and MBF decreased proportionately as ICF decreased in the range from 4 to 0 ml/min. Hypoxia significantly increased the rise in renal nerve activity (RNA) and CIR caused by cerebral ischemia, while hyperoxia significantly decreased them. Hypercapnia had almost no influence on the increases in RNA and mean arterial pressure produced by cerebral ischemia. CIR showed a much higher correlation with changes in tissue PO2 than with the other factors. We examined how these factors interact to modify CIR and found that central hypoxia is the main factor in producing CIR.

Role of the medullary lateral tegmental field in reflex-mediated sympathoexcitation in cats

2004 ◽  
Vol 286 (3) ◽  
pp. R451-R464 ◽  
Author(s):  
Hakan S. Orer ◽  
Gerard L. Gebber ◽  
Shaun W. Phillips ◽  
Susan M. Barman
Keyword(s):  
Nmda Receptor ◽  
Nmda Receptors ◽  
Receptor Antagonist ◽  
Sympathetic Nerve Activity ◽  
Nmda Receptor Antagonist ◽  
Vagal Afferents ◽  
Reflex Pathways ◽  
Excitatory Responses ◽  
Stimulation Of

We tested the hypothesis that blockade of N-methyl-d-aspartate (NMDA) and non-NMDA receptors on medullary lateral tegmental field (LTF) neurons would reduce the sympathoexcitatory responses elicited by electrical stimulation of vagal, trigeminal, and sciatic afferents, posterior hypothalamus, and midbrain periaqueductal gray as well as by activation of arterial chemoreceptors with intravenous NaCN. Bilateral microinjection of a non-NMDA receptor antagonist into LTF of urethane-anesthetized cats significantly decreased vagal afferent-evoked excitatory responses in inferior cardiac and vertebral nerves to 29 ± 8 and 24 ± 6% of control ( n = 7), respectively. Likewise, blockade of non-NMDA receptors significantly reduced chemoreceptor reflex-induced increases in inferior cardiac (from 210 ± 22 to 129 ± 13% of control; n = 4) and vertebral nerves (from 253 ± 41 to 154 ± 20% of control; n = 7) and mean arterial pressure (from 39 ± 7 to 21 ± 5 mmHg; n = 8). Microinjection of muscimol, but not an NMDA receptor antagonist, caused similar attenuation of these excitatory responses. Sympathoexcitatory responses to the other stimuli were not attenuated by microinjection of a non-NMDA receptor antagonist or muscimol into LTF. In fact, excitatory responses elicited by stimulation of trigeminal, and in some cases sciatic, afferents were enhanced. These data reveal two new roles for the LTF in control of sympathetic nerve activity in cats. One, LTF neurons are involved in mediating sympathoexcitation elicited by activation of vagal afferents and arterial chemoreceptors, primarily via activation of non-NMDA receptors. Two, non-NMDA receptor-mediated activation of other LTF neurons tonically suppresses transmission in trigeminal-sympathetic and sciatic-sympathetic reflex pathways.

Stimulation of the caudal ventrolateral medulla decreases total lung resistance in dogs

1987 ◽  
Vol 63 (3) ◽  
pp. 912-917 ◽  
Author(s):  
J. C. Connelly ◽  
L. W. McCallister ◽  
M. P. Kaufman
Keyword(s):  
Electrical Stimulation ◽  
Nucleus Ambiguus ◽  
Ventrolateral Medulla ◽  
Adrenergic Blockade ◽  
Homocysteic Acid ◽  
Caudal Ventrolateral Medulla ◽  
Airway Caliber ◽  
Lung Resistance ◽  
Total Lung Resistance ◽  
Stimulation Of

Although the role played by the caudal ventrolateral medulla in the regulation of the cardiovascular system has been extensively investigated, little is known about the role played by this area in the regulation of airway caliber. Therefore, in alpha-chloralose-anesthetized dogs, we used both electrical and chemical means to stimulate the caudal ventrolateral medulla while we monitored changes in total lung resistance breath by breath. We found that electrical stimulation (25 microA) of 26 sites in this area significantly decreased total lung resistance from 7.1 +/- 0.4 to 5.7 +/- 0.3 cmH2O.1'1.s (P less than 0.001). The bronchodilation evoked by electrical stimulation was unaffected by beta-adrenergic blockade but was abolished by cholinergic blockade. In addition, chemical stimulation of seven sites in the caudal ventrolateral medulla with microinjections of DL-homocysteic acid (0.2 M; 66 nl), which stimulates cell bodies but not fibers of passage, also decreased total lung resistance from 8.3 +/- 1.1 to 6.5 +/- 0.8 cmH2O.l'1.s (P less than 0.01). In contrast, microinjections of DL-homocysteic acid into the nucleus ambiguus (n = 6) increased total lung resistance from 7.5 +/- 0.5 to 9.2 +/- 0.4 cmH2O.l'1.s (P less than 0.05). We conclude that the caudal ventrolateral medulla contains a pool of cell bodies whose excitation causes bronchodilation by withdrawing cholinergic input to airway smooth muscle.

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