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.

Discharge patterns of ventrolateral medullary neurons during muscular contraction

1990 ◽  
Vol 259 (3) ◽  
pp. R606-R611 ◽  
Author(s):  
R. M. Bauer ◽  
G. A. Iwamoto ◽  
T. G. Waldrop
Keyword(s):  
Arterial Pressure ◽  
Minute Ventilation ◽  
Rapid Onset ◽  
Muscular Contraction ◽  
Firing Frequency ◽  
Ventrolateral Medulla ◽  
The Central Nervous System ◽  
Pressor Reflex ◽  
Discharge Patterns ◽  
Onset Response

Static muscular contraction is known to elicit reflex increases in arterial pressure. However, the areas of the central nervous system that mediate this reflex remain elusive. A recent study from this laboratory suggested that neurons in the ventrolateral medulla (VLM) participate in the pressor reflex to muscular contraction. In the present study, we sought to ascertain whether extracellular single-unit activity of VLM neurons is altered by static contraction of hindlimb muscles. In anesthetized cats, muscular contraction elicited by stimulation of L7 and S1 ventral roots evoked increases in arterial pressure, heart rate, and minute ventilation. The firing frequency in 33 of 50 VLM units increased greater than 70% during muscular contraction. VLM units displayed two types of discharge patterns in response to contraction: 1) a rapid onset response (0.5-3 s) and 2) a delayed onset response (10-20 s). Computer averaging analysis showed that 14 of 28 VLM units tested had a cardiac-related rhythm and 10 of those 14 also responded to muscular contraction. Muscular contraction had no effect on the discharge patterns of most neurons located outside the VLM. These findings suggest that neurons in the ventrolateral medulla respond to muscular contraction and may have a role in the pressor reflex to muscular contraction.

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.

Pressor response from rostral dorsomedial medulla is mediated by excitatory amino acid receptors in rostral VLM

1994 ◽  
Vol 267 (1) ◽  
pp. R309-R315 ◽  
Author(s):  
Y. Hirooka ◽  
J. W. Polson ◽  
R. A. Dampney
Keyword(s):  
Amino Acid ◽  
Excitatory Amino Acid ◽  
Pressor Response ◽  
Ventrolateral Medulla ◽  
Amino Acid Receptors ◽  
Control Value ◽  
Afferent Fibers ◽  
Pressor Responses ◽  
Before And After ◽  
Stimulation Of

Excitatory amino acid (EAA) receptors in the rostral part of the ventrolateral medulla (VLM) have been shown to mediate pressor responses elicited by stimulation of various peripheral afferent fibers as well as other central nuclei. This study tested the hypothesis that these receptors are a critical component in the central pathway mediating the powerful pressor response that is produced by stimulation of a group of neurons within a circumscribed region in the rostral dorsomedial medulla (RDM). In anesthetized rabbits, the pressor response elicited by unilateral microinjection of glutamate into this RDM region was measured before and after injection of kynurenic acid (Kyn), a broad-spectrum EAA receptor antagonist, into the physiologically identified pressor region of either the ipsilateral or contralateral rostral VLM. The pressor response to RDM stimulation was greatly reduced (to 24 +/- 4% of control) 5-10 min after injection of Kyn (but not the vehicle solution) into the ipsilateral rostral VLM; this response returned completely to its control value within 30-60 min after Kyn injection. By contrast, after Kyn injection into the contralateral rostral VLM, the pressor response to RDM stimulation was not affected (106 +/- 15% of control). The results indicate that the descending pressor pathway from the RDM to the spinal cord is mediated by EAA receptors in the rostral VLM pressor region. Furthermore, the pathway from the RDM to the rostral VLM is predominantly, if not exclusively, ipsilateral.

scholarly journals NADPH oxidase-derived reactive oxygen species in skeletal muscle modulates the exercise pressor reflex

2009 ◽  
Vol 107 (2) ◽  
pp. 450-459 ◽  
Author(s):  
Han-Jun Wang ◽  
Yan-Xia Pan ◽  
Wei-Zhong Wang ◽  
Irving H. Zucker ◽  
Wei Wang
Keyword(s):  
Blood Pressure ◽  
Reactive Oxygen Species ◽  
Nadph Oxidase ◽  
Pressor Response ◽  
Oxidase Inhibitor ◽  
Oxygen Species ◽  
Exercise Pressor Reflex ◽  
Pressor Reflex ◽  
Stimulation Of

Muscle metabolic by-products during exercise, such as K+, lactic acid, ATP, H+, and phosphate, are well established to be involved in the reflex cardiovascular response to static muscle contraction. However, the role of muscle reactive oxygen species (ROS), a metabolic by-product during muscle contraction, in the exercise pressor reflex (EPR) has not been investigated in detail. In the present study, we evaluated the role of muscle ROS in the EPR in a decerebrate rat model. We hypothesized that muscle NADPH oxidase-derived ROS contributes to sensitization of the EPR. Thus the rise in blood pressure and heart rate in response to a 30-s static contraction induced by electrical stimulation of L4/L5 ventral roots was compared before and after hindlimb arterial infusion of the redox agents: diethyldithiocarbamate, a superoxide dismutase inhibitor; the superoxide dismutase mimetic 4-hydroxy-2,2,6,6-tetramethyl piperidine 1-oxyl (tempol); the free radical scavenger dimethylthiourea; a NADPH oxidase inhibitor, apocynin; and a xanthine oxidase inhibitor, allopurinol. The EPR-induced pressor response was augmented after treatment with diethyldithiocarbamate and was attenuated after treatment with tempol, dimethylthiourea, and apocynin. Treatment with allopurinol did not affect the EPR function. None of the drug's affected the EPR heart rate response. In addition, neither the pressor response to electrical stimulation of the central end of dorsal roots, nor femoral blood flow was affected by any treatment. These data suggest that NADPH oxidase-derived muscle ROS plays an excitatory role in the EPR control of blood pressure.

Caudal ventrolateral medullary cells responsive to muscular contraction

1987 ◽  
Vol 62 (1) ◽  
pp. 149-157 ◽  
Author(s):  
G. A. Iwamoto ◽  
M. P. Kaufman
Keyword(s):  
Pressor Response ◽  
Receptive Fields ◽  
Muscular Contraction ◽  
Ventral Root ◽  
Nucleus Ambiguus ◽  
Ventrolateral Medulla ◽  
Reticular Nucleus ◽  
Metabolic Labeling ◽  
Response Patterns ◽  
Pressor Reflex

The pressor reflex evoked by muscular contraction (exercise pressor reflex) is held to be an important mechanism in producing the cardiovascular adjustments to static exercise. Recent experiments using lesioning and metabolic labeling methods have indicated that the caudal ventrolateral medulla may be a key integrative site for the reflex evoked by muscular contraction induced by ventral root stimulation. Therefore, we sought to determine whether cells in this region could be associated with the cardiovascular reflex accompanying muscular contraction through analysis of their discharge characteristics. Eighty cells were characterized as to their response to ventral root stimulus-induced static muscular contraction, intra-arterial capsaicin (selective groups III and IV stimulus), and mechanical probing. The cells' receptive fields were also determined by mechanical probing. The receptive fields were usually large, often including all four limbs and the trunk. Four response patterns were observed to static contractions: a brisk initial discharge followed by a gradual return toward control levels (slowly adapting), a brief onset and cessation response, a brief inhibition followed by a slowly adapting discharge, and inhibition alone. Virtually all cells tested were responsive to capsaicin. Histological analysis verified the position of the recorded cells. It is suggested that the cells most likely to participate in the pressor response to muscular contraction were those cells in the general region of the lateral reticular nucleus which responded with an initial and sustained discharge and the cells that were inhibited in the region of the nucleus ambiguus (possible inhibition of vagal outflow).

Role of ventrolateral medulla in vasomotor response to cerebral ischemia

1980 ◽  
Vol 239 (3) ◽  
pp. H349-H358 ◽  
Author(s):  
R. A. Dampney ◽  
E. A. Moon
Keyword(s):  
Cerebral Ischemia ◽  
Pressor Response ◽  
Ventrolateral Medulla ◽  
Medullary Reticular Formation ◽  
Norepinephrine Infusion ◽  
Pressor Responses ◽  
Highly Sensitive ◽  
Dorsal Medulla ◽  
Stimulation Of

The ventrolateral medulla has been postulated to contain chemosensitive neurons. This study investigated the role of this region in the generation of the pressor response to cerebral ischemia (CIR) in anesthetized paralyzed artificially ventilated rabbits. A circumscribed and highly sensitive pressor area in the ventrolateral medullary reticular formation 2-4 mm rostral to the obex, separate from the well-known dorsal pressor area, was mapped by use of a stimulating electrode. Electrolytic destruction of this area resulted in a profound reduction in resting mean arterial pressure (MAP). After restoration of baseline MAP with norepinephrine infusion, the CIR was greatly reduced (by mean 70.2% of control), but pressor responses from the dorsal medulla were unaffected. In contrast, lesions of greater size placed in the ventrolateral medulla more caudally did not significantly alter resting MAP and only slightly reduced the CIR (by mean 17.0% of control). Vasomotor responses to stimulation of the ventrolateral pressor area were unaffected by caudal ventrolateral lesions, but greatly reduced by dorsomedial lesions in the same plane. It is concluded that the ventrolateral area is either the site of origin or an essential part of the central vasomotor pathway mediating the CIR and that this pathway projects dorsomedially before descending to the spinal cord.

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.

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.

scholarly journals Developmental Changes in Hemodynamic Responses and Cardiovagal Modulation during Isometric Handgrip Exercise

2010 ◽  
Vol 2010 ◽  
pp. 1-11 ◽  
Author(s):  
Styliani Goulopoulou ◽  
Bo Fernhall ◽  
Jill A. Kanaley
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Isometric Contraction ◽  
Pressor Response ◽  
Reflex Response ◽  
Group Differences ◽  
Handgrip Exercise ◽  
Isometric Handgrip ◽  
Isometric Handgrip Exercise ◽  
Pressor Reflex

The purpose of this study was to examine differences in pressor response and cardiovagal modulation during isometric handgrip exercise (IHG) between children and adults. Beat-to-beat heart rate (HR) and blood pressure were measured in 23 prepubertal children and 23 adults at baseline and during IHG. Cardiovagal modulation was quantified by analysis of HR variability. Mean arterial pressure responses to IHG were greater in adults compared to children (P<.05) whereas there were no group differences in HR responses (P>.05). Children had a greater reduction in cardiovagal modulation in response to IHG compared to adults (P<.05). Changes in mean arterial pressure during IHG were correlated with baseline cardiovagal modulation and force produced during isometric contraction (P<.05). In conclusion, differences in pressor reflex response between children and adults cannot be solely explained by differences in autonomic modulation and appear to be associated with factors contributing to the force produced during isometric contraction.

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