Interactions between sympathetic and vagal cardiac afferents in nucleus tractus solitarii

1997 ◽  
Vol 272 (6) ◽  
pp. H2843-H2851 ◽  
Author(s):  
S. Tjen-A-Looi ◽  
A. Bonham ◽  
J. Longhurst
Keyword(s):  
Unit Activity ◽  
Pressor Response ◽  
Nucleus Tractus Solitarii ◽  
Vagal Afferents ◽  
Afferent Pathways ◽  
Before And After ◽  
The Central Nervous System ◽  
Afferent Inputs ◽  
Cardiac Afferents ◽  
Alpha Chloralose

Epicardial application of hydrogen peroxide (H2O2) reflexly elicits a sympathetically mediated pressor response. This pressor response is augmented by vagotomy and abolished by sympathectomy, suggesting an occlusive interaction between the afferents in the central nervous system (CNS). To support this observation we recorded sympathetic efferent responses from the sympathetic chain (T1-T2) before and after epicardial application of H2O2 in six cats before and after vagotomy. Cardiac sympathetic efferent responses to H2O2 were increased by vagotomy. Thus there exists an occlusive interaction between the two afferent pathways in the CNS. Because cardiopulmonary vagal afferents make their first central synapse in the nucleus tractus solitarii (NTS), we further hypothesized that cells in the NTS receive convergent inputs from sympathetic and vagal afferents and that the inputs would interact in an occlusive manner. In alpha-chloralose-anesthetized sinoaortic-denervated cats, cardiac sympathetic and vagal branches were stimulated electrically at 1 Hz, either separately or in combination. Extracellular single-unit activity was recorded in the NTS. Vagal stimuli most frequently (38%) diminished sympathetically evoked unit activity (-46.6 +/- 6.0%) versus control (1.4 +/- 1.5%). However, a few (21%) vagal and sympathetic afferent inputs were found to be additive or facilitative. We conclude that interactions occur between cardiac sympathetic and vagal afferents in the NTS. It is possible that this occlusive interaction explains the alteration in cardiac sympathetic outflow after epicardial stimulation with H2O2.

Responses and Afferent Pathways of Superficial and Deeper C1–C2 Spinal Cells to Intrapericardial Algogenic Chemicals in Rats

2001 ◽  
Vol 85 (4) ◽  
pp. 1522-1532 ◽  
Author(s):  
Chao Qin ◽  
Margaret J. Chandler ◽  
Kenneth E. Miller ◽  
Robert D. Foreman
Keyword(s):  
Afferent Input ◽  
Vagal Afferents ◽  
Male Rats ◽  
Prostaglandin E ◽  
Joint Movement ◽  
Spinal Neurons ◽  
Afferent Pathways ◽  
Bilateral Vagotomy ◽  
Cardiac Afferents ◽  
Stimulation Of

Electrical stimulation of vagal afferents or cardiopulmonary sympathetic afferent fibers excites C1–C2spinal neurons. The purposes of this study were to compare the responses of superficial (depth <0.35 mm) and deeper C1–C2 spinal neurons to noxious chemical stimulation of cardiac afferents and determine the relative contribution of vagal and sympathetic afferent pathways for transmission of noxious cardiac afferent input to C1–C2 neurons. Extracellular potentials of single C1–C2 neurons were recorded in pentobarbital anesthetized and paralyzed male rats. A catheter was placed in the pericardial sac to administer a mixture of algogenic chemicals (0.2 ml) that contained adenosine (10− 3 M), bradykinin, histamine, serotonin, and prostaglandin E2(10− 5 M each). Intrapericardial chemicals changed the activity of 20/106 (19%) C1–C2 spinal neurons in the superficial laminae, whereas 76/147 (52%) deeper neurons responded to cardiac noxious input ( P < 0.01). Of 96 neurons responsive to cardiac inputs, 48 (50%) were excited (E), 41 (43%) were inhibited (I), and 7 were excited/inhibited (E-I) by intrapericardial chemicals. E or I neurons responsive to intrapericardial chemicals were subdivided into two groups: short-lasting (SL) and long-lasting (LL) response patterns. In superficial gray matter, excitatory responses to cardiac inputs were more likely to be LL-E than SL-E neurons. Mechanical stimulation of the somatic field from the head, neck, and shoulder areas excited 85 of 95 (89%) C1–C2 spinal neurons that responded to intrapericardial chemicals; 31 neurons were classified as wide dynamic range, 49 were high threshold, 5 responded only to joint movement, and no neuron was classified as low threshold. For superficial neurons, 53% had small somatic fields and 21% had bilateral fields. In contrast, 31% of the deeper neurons had small somatic fields and 46% had bilateral fields. Ipsilateral cervical vagotomy interrupted cardiac noxious input to 8/30 (6 E, 2 I) neurons; sequential transection of the contralateral cervical vagus nerve (bilateral vagotomy) eliminated the responses to intrapericardial chemicals in 4/22 (3 E, 1 I) neurons. Spinal transection at C6–C7 segments to interrupt effects of sympathetic afferent input abolished responses to cardiac input in 10/10 (7 E, 3 I) neurons that still responded after bilateral vagotomy. Results of this study support the concept that C1–C2 superficial and deeper spinal neurons play a role in integrating cardiac noxious inputs that travel in both the cervical vagal and/or thoracic sympathetic afferent nerves.

Role of vagal afferents in the control of abdominal expiratory muscle activity in the dog

1991 ◽  
Vol 71 (5) ◽  
pp. 1795-1800 ◽  
Author(s):  
S. B. Hollstien ◽  
M. L. Carl ◽  
E. S. Schelegle ◽  
J. F. Green
Keyword(s):  
Muscle Activity ◽  
Vagal Afferents ◽  
Oblique Muscle ◽  
Vagus Nerves ◽  
Expiratory Muscle ◽  
C Fibers ◽  
C Fiber ◽  
Before And After ◽  
Afferent Vagal ◽  
Alpha Chloralose

We examined the contribution of afferent vagal A- and C-fibers on abdominal expiratory muscle activity (EMA). In seven spontaneously breathing supine dogs anesthetized with alpha-chloralose we recorded the electromyogram of the external oblique muscle at various vagal temperatures before and after the induction of a pneumothorax. When myelinated fibers were blocked selectively by cooling the vagus nerves to 7 degrees C, EMA decreased to 40% of control (EMA at 39 degrees C). With further cooling to 0 degrees C, removing afferent vagal C-fiber activity, EMA returned to 72% of control. On rewarming the vagus nerves to 39 degrees C, we then induced a pneumothorax (27 ml/kg) that eliminated the EMA in all the dogs studied. Cooling the vagus nerves to 7 degrees C, during the pneumothorax, produced a slight though not significant increase in EMA. However, further cooling of the vagus nerves to 0 degrees C caused the EMA to return vigorously to 116% of control. In three dogs, intravenous infusion of a constant incrementally increasing dose of capsaicin, a C-fiber stimulant, decreased EMA in proportion to the dose delivered. These results suggest that EMA is modulated by a balance between excitatory vagal A-fiber activity, most likely from slowly adapting pulmonary stretch receptors, and inhibitory C-fiber activity, most likely from lung C-fibers.

Expiratory abdominal muscle activity during ventilatory chemostimulation in piglets

1990 ◽  
Vol 68 (4) ◽  
pp. 1343-1349 ◽  
Author(s):  
J. F. Watchko ◽  
T. L. O'Day ◽  
B. S. Brozanski ◽  
R. D. Guthrie
Keyword(s):  
Abdominal Muscle ◽  
Vagal Afferents ◽  
Emg Activity ◽  
Abdominal Muscles ◽  
Base Line ◽  
Afferent Pathways ◽  
Newborn Piglets ◽  
Before And After ◽  
Cervical Vagotomy ◽  
Time Average

We examined abdominal muscle minute electromyographic (EMG) activity (peak moving time average EMG x respiratory rate) during eupnea, hyperoxic hypercapnia (8% CO2-40% O2-balance N2), and hypoxia (13% O2) in 12 anesthetized (0.5% halothane) newborn piglets. In addition, we assessed the role of vagal afferent pathways in the abdominal muscles' response to ventilatory chemostimulation by examining abdominal EMG activity (EMGab) before and after bilateral cervical vagotomy in five animals. Phasic expiratory EMGab was observed in 11 of 12 piglets during eupnea. Hypercapnia was associated with a sustained augmentation of minute EMGab (444 +/- 208% control). In contrast, hypoxia consistently augmented (1 min, 193 +/- 33% control) then diminished (5 min, 126 +/- 39% control) minute EMGab. Vagotomy resulted in a decline in peak moving time average EMGab by approximately one-half (48 +/- 18% control); the abdominal muscles' response to ventilatory chemostimulation, however, was qualitatively unchanged. We conclude that 1) expiration during eupnea in anesthetized newborn piglets is associated with phasic EMGab; 2) both hypercapnia and hypoxia augment minute EMGab; however, only hypercapnia is associated with sustained augmentation; and 3) although vagal afferents have a role in modulating the base-line level of EMGab, other extravagal mechanisms appear to determine the pattern of EMGab in response to ventilatory chemostimulation.

Regional vascular resistance during exercise: role of cardiac afferents and exercise training

1990 ◽  
Vol 258 (3) ◽  
pp. H842-H847 ◽  
Author(s):  
S. E. DiCarlo ◽  
V. S. Bishop
Keyword(s):  
Exercise Training ◽  
Vascular Resistance ◽  
Endurance Exercise ◽  
Vagal Afferents ◽  
Inhibitory Influence ◽  
Endurance Exercise Training ◽  
Exercise Training Program ◽  
Before And After ◽  
Regional Vascular Resistance ◽  
Cardiac Afferents

This study was designed to determine whether cardiac vagal afferents exert an inhibitory influence on increases in regional vascular resistance during exercise and to determine whether endurance exercise training enhances the inhibitory influence of cardiac vagal afferents. We measured changes in regional vascular resistance in 12 rabbits at rest and during running at 12.6 m/min, 20% grade, before and after reversible denervation of cardiac afferents (intrapericardial procainamide HCl, 2%). In addition, these procedures were repeated in five of these rabbits following an 8-wk endurance exercise training program. Because intrapericardial injections of procainamide anesthetize both the efferent as well as the afferent innervation to the heart, it was necessary to determine the effects of blocking the efferent innervation on the regulation of regional vascular resistance during exercise. Rabbits were instrumented with Doppler ultrasonic flow probes around the renal (R), mesenteric (M), ascending, and terminal aortic (TA) arteries. Catheters were positioned in the central ear artery and vein and pericardial sac. Mean arterial pressure, heart rate, cardiac output, R, M, TA, and systemic (S) resistances were determined. Exercise changed R (+37 +/- 4%), M (+88 +/- 9%), TA (-62 +/- 6%), and S (-34 +/- 3) resistances. Subsequent cardiac efferent blockade alone had no significant effect on regional vascular resistance during exercise. Combined efferent and afferent blockade resulted in significant increases in R (+62 +/- 6%) and M resistance (+134 +/- 13%) but did not alter TA (-51 +/- 4%) or S (-27 +/- 2%) resistance during exercise. Exercise training significantly enhanced the inhibitory influence of cardiac afferents on R and M regional vascular resistance.(ABSTRACT TRUNCATED AT 250 WORDS)

Vagal modulation of intestinal afferent sensitivity to systemic LPS in the rat

2007 ◽  
Vol 292 (5) ◽  
pp. G1213-G1220 ◽  
Author(s):  
C. Y. Liu ◽  
M. H. Mueller ◽  
D. Grundy ◽  
M. E. Kreis
Keyword(s):  
Systemic Blood Pressure ◽  
Feedback Mechanism ◽  
Afferent Nerve ◽  
Vagal Afferents ◽  
Partial Recovery ◽  
Before And After ◽  
The Central Nervous System ◽  
Vagal Afferent ◽  
Nerve Discharge

The central nervous system modulates inflammation in the gastrointestinal tract via efferent vagal pathways. We hypothesized that these vagal efferents receive synaptic input from vagal afferents, representing an autonomic feedback mechanism. The consequence of this vagovagal reflex for afferent signal generation in response to LPS was examined in the present study. Different modifications of the vagal innervation or sham procedures were performed in anesthetized rats. Extracellular mesenteric afferent nerve discharge and systemic blood pressure were recorded in vivo before and after systemic administration of LPS (6 mg/kg iv). Mesenteric afferent nerve discharge increased dramatically following LPS, which was unchanged when vagal efferent traffic was eliminated by acute vagotomy. In chronically vagotomized animals, to eliminate both vagal afferent and efferent traffic, the increase in afferent firing 3.5 min after LPS was reduced to 3.2 ± 2.5 impulses/s above baseline compared with 42.2 ± 2.0 impulses/s in controls ( P < 0.001). A similar effect was observed following perivagal capsaicin, which was used to eliminate vagal afferent traffic only. LPS also caused a transient hypotension (<10 min), a partial recovery, and then persistent hypertension that was exacerbated by all three procedures. Mechanosensitivity was increased 15 min following LPS but had recovered at 30 min in all subgroups except for the chronic vagotomy group. In conclusion, discharge in capsaicin-sensitive mesenteric vagal afferents is augmented following systemic LPS. This activity, through a vagovagal pathway, helps to attenuate the effects of septic shock. The persistent hypersensitivity to mechanical stimulation after chronic vagal denervation suggests that the vagus exerts a regulatory influence on spinal afferent sensitization following LPS.

Area postrema and aortic or vagal afferents converge to excite cells in nucleus tractus solitarius

1993 ◽  
Vol 264 (5) ◽  
pp. H1674-H1685 ◽  
Author(s):  
A. C. Bonham ◽  
E. M. Hasser
Keyword(s):  
Response Rate ◽  
Nucleus Tractus Solitarius ◽  
Area Postrema ◽  
Unit Response ◽  
Vagal Afferents ◽  
Afferent Pathways ◽  
Simple Addition ◽  
Aortic Depressor Nerve ◽  
Alpha Chloralose ◽  
Extracellular Activity

Area postrema neurons enhance baroreflex function, perhaps by augmenting baroreceptor afferent processing in the nucleus tractus solitarius (NTS). If so, NTS neurons should receive convergent excitatory inputs from area postrema neurons and baroreceptors. The aims of this study were to record extracellular activity of NTS neurons to determine whether 1) area postrema and aortic baroreceptor afferents converged in NTS, 2) area postrema and vagal afferents converged in NTS, and 3) the convergent inputs were facilitative. Studies were performed in pentobarbital sodium- or alpha-chloralose-anesthetized rabbits. Forty-six of 194 NTS neurons received inputs from the area postrema and aortic depressor nerve. Twelve of the 23 inputs showed facilitative summation; unit response rate evoked by paired inputs (79%) doubled the predicted (calculated) response rate for simple addition (37%). Fifty-eight of 114 NTS neurons received excitatory inputs from the area postrema and vagus. Eleven of the 13 inputs showed facilitative summation; unit response to paired inputs (87%) doubled the predicted response (44%). Area postrema neurons may augment the processing of aortic and vagal inputs by NTS neurons and, hence, enhance the reflex output of these afferent pathways.

Exogenous prostacyclin does not sensitize arterial baroreceptors

1991 ◽  
Vol 260 (6) ◽  
pp. H1760-H1766 ◽  
Author(s):  
Y. Hirooka ◽  
S. Ando ◽  
T. Imaizumi ◽  
S. Suzuki ◽  
A. Takeshita
Keyword(s):  
Aortic Pressure ◽  
Vagal Afferents ◽  
Nerve Activity ◽  
Arterial Baroreceptors ◽  
Background Infusion ◽  
Before And After ◽  
Bilateral Vagotomy ◽  
Alpha Chloralose ◽  
The Relationship ◽  
Cardiac Receptors

It has been shown that prostacyclin (PGI2) sensitizes cardiac receptors. However, the effects of PGI2 on arterial baroreceptors are not well understood. In rabbits anesthetized with alpha-chloralose (n = 12), we examined reflex changes in multiunit efferent renal sympathetic nerve activity (RSNA) during hypotension caused by intravenous PGI2 (0.1, 0.2, 0.5, 1.0, 2.0 micrograms/kg), nitroglycerin (NG; 5, 10, 20, 50, 100 micrograms/kg), and sodium nitroprusside (SNP; 5, 10, 20, 50, 100 micrograms/kg) before and after bilateral vagotomy. Before vagotomy, RSNA increased during hypotension caused by NG or SNP (P less than 0.01) but did not significantly change during comparable hypotension caused by PGI2. After vagotomy, PGI2 increased RSNA as much as NG or SNP. In another group (n = 6), we examined the changes in aortic pressure (AoP), multiunit afferent aortic nerve activity (ANA), and the aortic diameter (AoD) during hypotension caused by intravenous PGI2, NG, and SNP. The relationship between changes in AoP and those in ANA did not differ during hypotension caused by the three drugs. The relationship between changes in AoP and those in AoD and that between changes in AoD and those in ANA also did not differ. Finally, we examined changes in AoP, ANA, and AoD during ramp increases or decreases of AoP caused by intravenous angiotensin II or NG under background infusion of saline, PGI2, or SNP (n = 6). The relationship among these variables did not differ during infusion of PGI2 and SNP. These results suggest that PGI2 stimulates cardiac receptors with vagal afferents but does not sensitize arterial baroreceptors.

Central Nervous System Processing of Emotions in Children with Fecal Incontinence and Constipation

2019 ◽  
Vol 47 (1) ◽  
pp. 67-71
Author(s):  
Monika Equit ◽  
Justine Niemczyk ◽  
Anna Kluth ◽  
Carla Thomas ◽  
Mathias Rubly ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Fecal Incontinence ◽  
Event Related Potentials ◽  
Anterior Cingulate ◽  
Afferent Pathways ◽  
Study Results ◽  
Related Potentials ◽  
The Central Nervous System ◽  
Cortical Regions

Abstract. Objective: Fecal incontinence and constipation are common disorders in childhood. The enteric nervous system and the central nervous system are highly interactive along the brain-gut axis. The interaction is mainly afferent. These afferent pathways include centers that are involved in the central nervous processing of emotions as the mid/posterior insula and the anterior cingulate cortex. A previous study revealed altered processing of emotions in children with fecal incontinence. The present study replicates these results. Methods: In order to analyze the processing of emotions, we compared the event-related potentials of 25 children with fecal incontinence and constipation to those of 15 control children during the presentation of positive, negative, and neutral pictures. Results: Children with fecal incontinence and constipation showed altered processing of emotions, especially in the parietal and central cortical regions. Conclusions: The main study results of the previous study were replicated, increasing the certainty and validity of the findings.

Central blockade of vasopressin V1receptors attenuates postexercise hypotension

2001 ◽  
Vol 281 (2) ◽  
pp. R375-R380 ◽  
Author(s):  
Heidi L. Collins ◽  
David W. Rodenbaugh ◽  
Stephen E. DiCarlo
Keyword(s):  
Central Administration ◽  
Guide Cannula ◽  
Spontaneously Hypertensive ◽  
Single Bout ◽  
Before And After ◽  
The Central Nervous System ◽  
Postexercise Hypotension ◽  
The Right ◽  
Carotid Arterial ◽  
Lateral Cerebral Ventricle

We tested the hypothesis that central arginine vasopressin (AVP) mediates postexercise reductions in arterial pressure (AP) and heart rate (HR). To test this hypothesis, nine spontaneously hypertensive rats (SHR) were instrumented with a 22-gauge stainless steel guide cannula in the right lateral cerebral ventricle and with a carotid arterial catheter. After the rats recovered, AP and HR were assessed before and after a single bout of dynamic exercise with the central administration of vehicle or the selective AVP V1-receptor antagonist d(CH3)5Tyr(Me)-AVP (AVP-X). AP and HR were significantly decreased below preexercise values with central administration of vehicle [ P < 0.05, change (Δ)−21 ± 4 mmHg and Δ−20 ± 6 beats/min, respectively]. In sharp contrast, after exercise with central administration of AVP-X, both AP (Δ+8 ± 5 mmHg) and HR (Δ+24 ± 9 beats/min) were not significantly different from preexercise values ( P > 0.05). Furthermore, AVP-X at rest did not significantly alter AP (181 ± 11 vs. 178 ± 11 mmHg, P > 0.05) or HR (328 ± 24 vs. 331 ± 22 beats/min, P > 0.05). Thus central blockade of AVP V1 receptors prevented postexercise reductions in AP and HR. These data suggest that AVP, acting within the central nervous system, mediates postexercise reductions in AP and HR in the SHR.

Intravenous morphine-induced activation of vagal afferents: peripheral, spinal, and CNS substrates mediating inhibition of spinal nociception and cardiovascular responses

1992 ◽  
Vol 68 (4) ◽  
pp. 1027-1045 ◽  
Author(s):  
A. Randich ◽  
C. L. Thurston ◽  
P. S. Ludwig ◽  
J. D. Robertson ◽  
C. Rasmussen
Keyword(s):  
Intravenous Administration ◽  
Pressor Response ◽  
Cardiovascular Responses ◽  
Ibotenic Acid ◽  
Vagal Afferents ◽  
Spinothalamic Tract ◽  
Depressor Response ◽  
Arterial Blood ◽  
Intravenous Morphine ◽  
Cervical Vagotomy

1. Intravenous administration of 1.0 mg/kg of morphine produces inhibition of the nociceptive tail-flick (TF) reflex, hypotension, and bradycardia in the pentobarbital-anesthetized rat. The present experiments examined peripheral, spinal, and supraspinal relays for inhibition of the TF reflex and cardiovascular responses produced by morphine (1.0 mg/kg iv) in the pentobarbital-anesthetized rat using 1) bilateral cervical vagotomy, 2) spinal cold block or mechanical lesions of the dorsolateral funiculi (DLFs), or 3) nonselective local anesthesia or soma-selective lesions of specific CNS regions. Intravenous morphine-induced inhibition of responses of unidentified, ascending, and spinothalamic tract (STT) lumbosacral spinal dorsal horn neurons to noxious heating of the hindpaw were also examined in intact and bilateral cervical vagotomized rats. 2. Bilateral cervical vagotomy significantly attenuated inhibition of the TF reflex and bradycardia produced by intravenous administration of morphine. Bilateral cervical vagogtomy changed the normal depressor response produced by morphine into a sustained pressor response. Inhibition of the TF reflex in intact rats was not due to changes in tail temperature. 3. Spinal cold block significantly attenuated inhibition of the TF reflex, the depressor response, and the bradycardia produced by intravenous administration of morphine. However, bilateral mechanical transections of the DLFs failed to significantly affect either inhibition of the TF reflex or cardiovascular responses produced by this dose of intravenous morphine. 4. Microinjection of either lidocaine or ibotenic acid into the nuclei tracti solitarii (NTS), rostromedial medulla (RMM), or ventrolateral pontine tegmentum (VLPT) attenuated morphine-induced inhibition of the TF reflex. Similar microinjections into either the periaqueductal gray (PAG) or the dorsolateral pons (DLP) failed to affect morphine-induced inhibition of the TF reflex. 5. Microinjection of either lidocaine or ibotenic acid into the NTS, RMM, VLPT, DLP, or rostral ventrolateral medulla (RVLM) attenuated the depressor response produced by morphine, although baseline arterial blood pressure (ABP) was affected by ibotenic acid microinjections in the DLP. In all these cases, the microinjections failed to reveal a sustained pressor response as was observed with bilateral cervical vagotomy. Similar microinjections into the PAG failed to affect the depressor response produced by morphine. 6. The lidocaine and ibotenic acid microinjection treatments also showed that the bradycardic response produced by morphine depends on the integrity of the NTS, RMM, RVLM, and possibly the DLP, but not the PAG or VLPT.(ABSTRACT TRUNCATED AT 400 WORDS)

Sign in / Sign up

Export Citation Format

Share Document