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1  ATP acts as an additional signal triggering vagal activation and potentially synergising with the ac
2 established reflex arc resulting in efferent vagal activity and asthmatic bronchoconstriction.
3 d post-inspiratory peaks in efferent cardiac vagal activity and suppressed RSA, whereas substantial c
4                 Indirect measures of cardiac vagal activity are strongly associated with exercise cap
5                                       Reflex vagal activity causes abrupt heart rate slowing with con
6 ncy component (0.15-0.4 Hz), an indicator of vagal activity, the low-frequency component (0.04-0.15 H
7  to efficiently oppose enhanced responses to vagal activity.
8 -intensity ES at hindlimb regions drives the vagal-adrenal axis, producing anti-inflammatory effects
9 ith functional or reflex bradyarrhythmias or vagal AF treated with AFN ablation and a control group (
10 evokes de novo adrenergic reflexes following vagal afferent activation.
11 ns like asthma, for its ability to stimulate vagal afferent C-fibres in mouse lungs.
12 ave been many anterograde tracing studies of vagal afferent endings, but none on spinal afferent endi
13 urons received monosynaptic innervation from vagal afferent fibers and LepR neurons exhibited large s
14 ity, these circadian fluctuations in gastric vagal afferent mechanosensitivity are lost.
15 ability of 5-HT to increase anterior gastric vagal afferent nerve (VAN) activity in vivo before and a
16 t HFD does not alter the response of gastric vagal afferent nerves and neurones to 5-HT but attenuate
17 esponsible for symptoms and are regulated by vagal afferent nerves, which innervate the airway.
18  about the secretory state of beta-cells via vagal afferent nerves.
19                  To test the hypothesis that vagal afferent neuron (VAN) GLP-1 receptors (GLP-1Rs) ar
20                                              Vagal afferent neuron (VAN) signaling sends information
21 y and function of 5-HT3 receptors on gastric vagal afferent neurones.
22         Depending on the nutritional status, vagal afferent neurons express two different neurochemic
23          Single cell RT-PCR on lung-specific vagal afferent neurons revealed that both TRPV1-expressi
24 of calorie-rich diets reduces sensitivity of vagal afferent neurons to peripheral signals and their c
25 ctor, acting at type 1 receptors (CCK1Rs) on vagal afferent neurons; however, CCK agonists have faile
26   Patients with diabetes have defects in the vagal afferent pathway that result in abnormal gastroint
27 coming anorexigenic signals that act via the vagal afferent pathways.
28 anilloid type-4 (TRPV4) mechanoreceptors and vagal afferent purinergic receptors (P2X) act as trigger
29 ility in TNX deficient mice, suggesting that vagal afferent responses are probably the result of alte
30 ated gastric emptying and markedly increased vagal afferent responses to gastric distension that coul
31 rst evidence that diet-induced disruption to vagal afferent signaling may cause a perturbation in cir
32 These results suggest that glucose-dependent vagal afferent signalling is compromised by relatively s
33         This suggests that glucose-dependent vagal afferent signalling is compromised by short period
34                           This disruption of vagal afferent signalling is sufficient to drive hyperph
35 hitecture TNX is associated exclusively with vagal-afferent endings and some myenteric neurones in mo
36 rs that can be normalized by an inhibitor of vagal-afferent sensitivity.
37                                      Gastric vagal afferents (GVAs) respond to mechanical stimuli to
38  of its extremities, it contained a mixed of vagal afferents and postganglionic sympathetic neurons.
39 PV4 in mediating sensory nerve activation in vagal afferents and the possible downstream signaling me
40                                              Vagal afferents are involved in regulation of feeding be
41    Leptin receptors (LepRs) are expressed by vagal afferents as well as by a population of NTS neuron
42  in SH rats, and this reflex is dependent on vagal afferents but is not due to steady state blood pre
43  be a consequence of increased activation of vagal afferents by pathology in the airways (e.g., infla
44  different temporal characteristics and that vagal afferents enhance parasympathetic and reduce sympa
45 ed that in insulin-resistant animals, portal vagal afferents failed to inhibit their spiking activity
46  of the solitary tract (NTS) is activated by vagal afferents from the gastrointestinal tract, which p
47           These studies clarify the roles of vagal afferents in mediating particular gut hormone resp
48 rated a long sought-after molecular atlas of vagal afferents in the mouse.
49                                              Vagal afferents innervating the small intestinal mucosa
50 th markers of postganglionic sympathetic and vagal afferents neurons.
51                               Stimulation of vagal afferents or efferents in mice 24 hours before IRI
52 dent modulation of 5-HT responses in gastric vagal afferents prior to the development of obesity.
53 dent modulation of 5-HT responses in gastric vagal afferents prior to the development of obesity.
54 e brain of changes in glucose inflow through vagal afferents that require an activated glucagon-like
55 molecules into the CNS, and/or activation of vagal afferents that trigger CNS inflammation.
56 ot affect the response of gastric-projecting vagal afferents to 5-HT, it attenuates the ability of gl
57 ity attenuates the responsiveness of gastric vagal afferents to several neurohormones, the aim of the
58                                              Vagal afferents were found to be organized into 24 subty
59 scussed with respect to studies of the mouse vagal afferents, an area of research of increasing popul
60 rt how primary visceral afferents, including vagal afferents, can maintain fidelity of transmission a
61 es are triggered by transmitters released by vagal afferents, glutamate acting at AMPA receptors and
62         During high-frequency stimulation of vagal afferents, leptin increased the size of NMDAR-medi
63                   For example, inhibitors of vagal afferents-baclofen could be beneficial in patients
64 mises the excitability and responsiveness of vagal afferents.
65                                      Jugular vagal airway sensory neurons wire into a brainstem circu
66                     ENS cells originate from vagal and sacral neural crest cells that are initially l
67 lly relevant example of intersection between vagal and somatosensory processing in the brain.
68 nses to stress, as well as direct input from vagal and spinal sensory neurons.
69 siological stress responses, as well as from vagal and spinal sensory neurons.
70 offer new insights into interactions between vagal and spinal sensory processing, including the medul
71  component (0.04-0.15 Hz), a mixture of both vagal and sympathetic activity, and the ratio of the low
72 erful reflex responses through activation of vagal and sympathetic afferents in the heart through the
73        There is an important and significant vagal and sympathetic denervation after 2 years of cardi
74 e moment of lung inflation accounts for both vagal and sympathetic influences.
75 this region reduced the amplitudes of post-I vagal and sympathetic nerve activities.
76 ted plasma corticosterone and increased both vagal and sympathetic nerve activity, C1-mediated IRI pr
77 ns as reflex/functional bradyarrhythmias and vagal atrial fibrillation (AF).
78 duction properties and might be critical for vagal attenuation.
79 sympathetic nerve activity, cardiac sympatho-vagal balance and arrhythmia incidence in an animal mode
80 mia incidence, and improves cardiac sympatho-vagal balance and breathing stability.
81 ing molecules that modulate cardiac sympatho-vagal balance in the progression of heart disease.
82 moreflex gain, cardiac function and sympatho-vagal balance, and arrhythmia incidence were studied.
83  and spectral indicators of cardiac sympatho-vagal balance.
84                                      Cardiac vagal baroreflex function was assessed using the modifie
85 agal metrics changed in opposite directions: vagal baroreflex gain and two indices of vagal fluctuati
86 agal metrics changed in opposite directions: vagal baroreflex gain and two indices of vagal fluctuati
87 ailed); altered arterial baroreceptor input (vagal baroreflex gain declined and muscle sympathetic ne
88                                              Vagal blockade is proposed to inhibit aberrant orexigeni
89                                              Vagal blockade, which inhibits the vagus nerve, results
90 rising in obesity as a putative mechanism of vagal blockade-induced weight loss.
91 identify three novel subpopulations of EGFP+ vagal brainstem neurons: (a) EGFP+ neurons in the nAmb p
92 ration, recordings from the cut left cardiac vagal branch showed efferent activity that peaked in pos
93 In separate preparations with intact cardiac vagal branches but sympathetically denervated by thoraci
94 triggered a pronounced stimulatory effect on vagal bronchopulmonary C-fibres in anaesthetized rats.
95 flex bronchoconstriction, and stimulation of vagal bronchopulmonary C-fibres is primarily responsible
96 esults obtained from studies in isolated rat vagal bronchopulmonary sensory neurones and also in the
97 ons Apnea increases GP activity, followed by vagal bursts and tonic stellate ganglion firing.
98                                              Vagal bursts remained unchanged.
99 GP activity, followed by clustered crescendo vagal bursts synchronized with heart rate and blood pres
100 e-1-phosphate (S1P) strongly activates mouse vagal C-fibres in the airways.
101 rs in the brain control heart activities and vagal cardiovascular reflexes involve purines.
102 cell RNA sequencing to generate a map of the vagal cell types that innervate the gastrointestinal tra
103  or molecular GlyT1 knockdown, in the dorsal vagal complex (DVC) suppresses glucose production, incre
104              Neurons in the brainstem dorsal vagal complex integrate neural and humoral signals to co
105  in the subpallium, hypothalamus, and dorsal vagal complex of birds suggests that some of the functio
106 way in rats, we placed tracers in the dorsal vagal complex or SNpc; brainstem and midbrain were exami
107 ith autonomic function, including the dorsal vagal complex, A5, rostral ventral medulla, A1, and midl
108 teatotic effects are generated in the dorsal vagal complex, require hepatic vagal innervation, and ar
109 vation of dopamine 1 receptors in the dorsal vagal complex.
110 ation of nigro-vagal terminals in the dorsal vagal complex.
111 uctal gray, parabrachial nucleus, and dorsal vagal complex.
112 enhancement in cFos-activation in the dorsal-vagal-complex (DVC) compared to mono-therapy, suggesting
113              These findings indicate reduced vagal control and impaired cardiovascular homeostasis du
114 ge tasks on cortical auditory processing and vagal control of heart rate and (2) to verify a possible
115 om the symptomatic MCs and from NMCs in less vagal control of heart rate and more reactive sympatheti
116 hese results indicate that glucose activates vagal control of hyperglycemia and inflammation in faste
117                              Reduced cardiac vagal control reflected in low heart rate variability (H
118 ic pressure, other autonomic functions under vagal control.
119                     Cardioneuroablation, the vagal denervation by radiofrequency ablation of the neur
120                This study aims to verify the vagal denervation degree in the chronic phase after card
121     Cardioneuroablation provides therapeutic vagal denervation through endocardial radiofrequency abl
122             ECVS was fundamental to stepwise vagal denervation validation during cardioneuroablation.
123                                              Vagal denervation was performed to assess its effect on
124  and critical atrial regions responsible for vagal denervation.
125       Non-AFN ablation causes no significant vagal denervation.
126              AFN ablation causes significant vagal denervation.
127 blation ECVS=P<0.0001), demonstrating robust vagal denervation.
128 olished the post-inspiratory peak of cardiac vagal discharge (and cyclical HR modulation), although a
129 t experimental evidence that parasympathetic vagal drive generated by a defined CNS circuit determine
130 hatidic acid elicits a reflex stimulation of vagal efferent activity sufficient to cause bronchoconst
131  the cardiac responses of WKY and SH rats to vagal efferent electrical stimulation.
132 tate blood pressure or due to remodelling of vagal efferent function.
133 Selective activation of afferent or efferent vagal fibers can maximize efficacy and minimize off-targ
134 ns: vagal baroreflex gain and two indices of vagal fluctuations (root mean square of successive norma
135 ns: vagal baroreflex gain and two indices of vagal fluctuations rose and then fell in space, and desc
136 onstrate that a population of neurons in the vagal ganglia and brainstem are activated via the gut-br
137                       The nodose and jugular vagal ganglia supply sensory innervation to the airways
138 vo vagus nerve and neuron cell bodies in the vagal ganglia.
139 ircuits in receipt of inputs from the nodose vagal ganglia.
140   We used genetic tools that broadly cover a vagal/glossopharyngeal sensory neuron atlas to map, abla
141 ological insight into heritable variation in vagal heart rhythm regulation, with a key role for genet
142                                              Vagal hyperactivity is directly related to several clini
143 ws in the first year, that could recover the vagal hyperactivity.
144 ates diastolic dysfunction, worsens sympatho-vagal imbalance and markedly increases the incidence of
145 HFpEF) display irregular breathing, sympatho-vagal imbalance, arrhythmias and diastolic dysfunction.
146  disordered breathing patterns, and sympatho-vagal imbalance.
147 on labeled in Na(v) 1.8-Cre-tdTomato mice is vagal in origin.
148 as alcohol signals hypothalamic neurons in a vagal-independent manner, while fat and satiation signal
149 rst confirm the presence of tonic inhibitory vagal influence on LV inotropy.
150 verity of fibrosis in lungs with and without vagal innervation in unilaterally vagotomized mice.
151 in the dorsal vagal complex, require hepatic vagal innervation, and are preserved in high-fat-diet-fe
152 ggest that AFNs are intrinsically related to vagal innervation.
153 bility suggests that they are related to the vagal innervation.
154 he sensitivity of LepR-expressing neurons to vagal inputs by increasing NMDA receptor-mediated synapt
155                                      Jugular vagal inputs to SubM via the medullary paratrigeminal nu
156  the solitary tract, which receives afferent vagal inputs.
157  currents, thus enhancing NTS sensitivity to vagal inputs.SIGNIFICANCE STATEMENT Leptin is a hormone
158 le morphological information is available on vagal intramuscular arrays (IMAs), the afferents that in
159  lobe mainly ending medially to those of the vagal lobe, and those from the commissural nucleus ventr
160  descending projections to the SGN/V and the vagal lobe.
161   Main primary gustatory centers (facial and vagal lobes) received sensory projections from the facia
162 la, and superficial layers of the facial and vagal lobes.
163 ric emptying and hypersensitivity of gastric vagal mechanoreceptors that can be normalized by an inhi
164                                              Vagal metrics changed in opposite directions: vagal baro
165                                              Vagal metrics changed in opposite directions: vagal baro
166 quency power (LF/HF) were used as indices of vagal modulation and sympathovagal balance.
167 ircadian misalignment decreased wake cardiac vagal modulation by 8-15%, as determined by heart rate v
168 sinus arrhythmia (RSA), a measure of cardiac vagal modulation, provides cardiac risk stratification i
169      We identified and characterized a nigro-vagal monosynaptic pathway in rats that controls gastric
170 nges reflected by reciptocal sympathetic and vagal motoneurone responsiveness to breathing changes.
171 ng their voltage-activated calcium channels, vagal motoneurons acquire a stressless form of pacemakin
172 to dopamine neurons in the substantia nigra, vagal motoneurons do not enhance their excitability and
173 rowth factor (HGF), by tissues innervated by vagal motor neurons during fetal development reveal pote
174 a suggest that MET+ neurons in the brainstem vagal motor nuclei are anatomically positioned to regula
175 ping of the viscerotopic organization of the vagal motor nuclei has provided insight into autonomic f
176 , trochlear, trigeminal motor, abducens, and vagal motor nuclei) contain protocadherin-19 and/or prot
177 c neurons residing in the brainstem's dorsal vagal motor nucleus dramatically impairs exercise capaci
178 re, these mice will be valuable for studying vagal mucosal afferent morphology, interactions with oth
179  enhanced heart rate responses of the SAN to vagal nerve activity in vivo.
180                                          The vagal nerve also projects to the commissural nucleus of
181                  Invasive stimulation of the vagal nerve previously demonstrated a reduced risk of PO
182 e) trial assessed the safety and efficacy of vagal nerve stimulation (VNS) among patients with HF and
183                                              Vagal nerve stimulation (VNS) is well established.
184 es, in patients with depression or epilepsy, vagal nerve stimulation has been demonstrated to promote
185 though the mechanisms are poorly understood, vagal nerve stimulation prevents weight gain in response
186                          Implantable cardiac vagal nerve stimulators are a promising treatment for ve
187                        In contrast, no lung, vagal nerve, or esophageal injury was observed at PFA si
188 iated by the injury to the components of the vagal nerve.
189 the respiratory motor pattern on phrenic and vagal nerves in the perfused brainstem preparation.
190                 These findings indicate that vagal nerves that release several neurotransmitters may
191              Nerve recordings from bilateral vagal nerves, left stellate ganglion, and anterior right
192 ived sensory projections from the facial and vagal nerves, respectively.
193 s system (ENS) predominantly originates from vagal neural crest (VNC) cells that emerge from the caud
194 ebrates, a role that was largely subsumed by vagal neural crest cells in early gnathostomes.
195 m of jawed vertebrates arises primarily from vagal neural crest cells that migrate to the foregut and
196                                              Vagal neurocircuits are vital to the regulation of upper
197 r pathway by which EECs regulate enteric and vagal neuronal pathways in response to microbial signals
198 ty of the gut-brain axis, and identified the vagal neurons activated by intestinal delivery of glucos
199                                   Centrally, vagal neurons projecting to the pancreas terminate in th
200       Patch clamp recordings of isolated rat vagal neurons show that ghrelin hyperpolarizes neurons b
201 tify a subset of distal intestine-projecting vagal neurons that are positioned to have an afferent ro
202  show that unique molecular markers identify vagal neurons with distinct innervation patterns, sensor
203 travel provokes long-lasting sympathetic and vagal neuroplastic changes in healthy humans.
204 tify the pathway that connects the brainstem vagal nuclei and the SNpc, and to determine whether this
205  serve as integrative targets for modulating vagal output activity to the stomach.
206                                  Ablation of vagal P2RY1 neurons eliminates protective responses to l
207                    Optogenetic activation of vagal P2RY1 neurons evokes a coordinated airway defense
208  common were carotid paragangliomas (59) and vagal paragangliomas (27).
209                                  Carotid and vagal paragangliomas occurred most often.
210 , 49 (59%) male, 47.3+/-17 years old, having vagal paroxysmal atrial fibrillation 58 (70%) or neuroca
211 at-induced model of Parkinsonism, this nigro-vagal pathway was compromised during the early stages of
212 ced inhibitory effect of Sst-GABA neurons on vagal pre-motor neurons in the DMV that control gastric
213 c control of LV contractility is provided by vagal preganglionic neurones located in the dorsal motor
214 eft ventricular contractility is provided by vagal preganglionic neurones of the dorsal motor nucleus
215 tional neuroanatomical mapping revealed that vagal preganglionic neurones that have an impact on left
216 ent of the left and right DVMN revealed that vagal preganglionic neurones, which have an impact on LV
217                          The activity of the vagal preganglionic neurons is predominantly regulated b
218 ncing of the largest population of brainstem vagal preganglionic neurons residing in the brainstem's
219 (DMV) in the brainstem consists primarily of vagal preganglionic neurons that innervate postganglioni
220 dic CJD and 7 of 30 genetic CJD cases showed vagal PrP(Sc) immunodeposits with distinct morphology.
221 stimulus threshold of the action currents of vagal pulmonary C-neurons, and 4) the immunoreactivity (
222                 Furthermore, in isolated rat vagal pulmonary sensory neurones, perfusion of an aqueou
223 refluxate with the upper airway or by a vago-vagal reflex.
224 uit exerts descending regulation over airway vagal reflexes in male and female rats using a range of
225                                              Vagal reflexes slow heart rate and can change where the
226 estinal motility, which are mediated by vago-vagal reflexes.
227 se neural crest leads to an altered sympatho-vagal regulation of cardiac rhythmicity in adults charac
228 icular block in both groups showing a strong vagal response (P=0.96).
229 p showed complete abolishment of the cardiac vagal response in all cases (pre/postablation ECVS=P<0.0
230               However, in the control group, vagal response remained practically unchanged postablati
231                                              Vagal response was evaluated before, during, and postabl
232            GP ablation abated 100% of evoked vagal responses; these responses remained in 87% of cont
233 ess is known about the mechanisms underlying vagal sensing itself.
234 nsitization with a consequent suppression of vagal sensitivity to portal glucose.
235 und that pancreatic islets are innervated by vagal sensory axons expressing Phox2b, substance P, calc
236 tivation of Trpa1(+)EECs directly stimulates vagal sensory ganglia and activates cholinergic enteric
237 ditionally, PPG neurons receive monosynaptic vagal sensory input from the nodose ganglia and spinal s
238 e, we investigate the molecular diversity of vagal sensory neurons and their roles in sensing gastroi
239          Optogenetic activation of Piezo2(+) vagal sensory neurons causes apnoea in adult mice.
240           Within the gastrointestinal tract, vagal sensory neurons detect gut hormones and organ dist
241  that pancreatic beta-cells communicate with vagal sensory neurons, likely using serotonin signaling
242 e functional interactions of beta-cells with vagal sensory neurons, we recorded Ca(2+) responses in i
243 2% and 22%, respectively) of airway-specific vagal sensory neurons; whereas S1PR4 and S1PR5 were rare
244 rganization suggests an intersection between vagal sensory pathways and the endogenous analgesia syst
245 ty in disease.SIGNIFICANCE STATEMENT Jugular vagal sensory pathways are increasingly recognized for t
246              These data suggest that jugular vagal sensory pathways input to a nociceptive thalamocor
247 tem, potentially important for understanding vagal sensory processing in health and mechanisms of hyp
248 ventilator-induced brain injury via afferent vagal signaling and hippocampal neurotransmitter imbalan
249                The triggering mechanisms for vagal signaling during mechanical ventilation are unknow
250 nt, determined conduction velocities of some vagal signals in the afferent (0.7-4.4 m/s) and efferent
251 mechanical responses to selective electrical vagal stimulation (EVS) were recorded from gastric fundu
252 ugh the internal jugular veins (extracardiac vagal stimulation [ECVS]), analyzing 15 s mean heart rat
253 , during, and postablation by 5 s noncontact vagal stimulation at the jugular foramen, through the in
254                                              Vagal stimulation attenuated hyperglycemia and serum TNF
255                     We conclude that chronic vagal stimulation improves insulin sensitivity substanti
256                                              Vagal stimulation induced the production of dopamine fro
257 abolism, but the effect of chronic bilateral vagal stimulation is not known.
258                                        Acute vagal stimulation modifies glucose and insulin metabolis
259 ivities 12 weeks after permanent, bilateral, vagal stimulation performed at the abdominal level in ad
260                                              Vagal stimulation was associated with increased glucose
261  of neuronal activation in the PVH following vagal stimulation, and whole-cell patch recordings of GL
262 released from G-protein-coupled receptors on vagal stimulation.
263  neurohumoral modification by baroreflex and vagal stimulation; prevention of adverse cardiac remodel
264              We found that disruption of the vagal system in mice delayed resolution of Escherichia c
265 SNpc and/or optogenetic stimulation of nigro-vagal terminals in the dorsal vagal complex.
266 ime the influence of disinhibited eating and vagal tone (heart rate variability (HRV)) on hunger and
267                     Substantial chronotropic vagal tone also remained after transection of the brains
268 how that over-activation of sgACC/25 reduces vagal tone and heart rate variability, alters cortisol d
269 sized that respiratory modulation of cardiac vagal tone and HR is intrinsically linked to the generat
270                           Arterial pressure, vagal tone and muscle sympathetic outflow were comparabl
271 t-brainstem preparation shows strong cardiac vagal tone and pronounced respiratory sinus arrhythmia.
272  is associated with reduced baseline cardiac vagal tone and that this reduction correlates with left-
273                     The depression of cardio-vagal tone and the shift toward a sympathetic predominan
274  are important for the regulation of cardiac vagal tone are not clear.
275                     We conclude that cardiac vagal tone depends on neurons in at least three sites of
276                     We conclude that cardiac vagal tone depends upon at least 3 sites of the pontomed
277 enatal exposure to PM2.5 may disrupt cardiac vagal tone during infancy.
278   Respiratory-linked fluctuations in cardiac vagal tone give rise to respiratory sinus arryhthmia (RS
279                                 (INcrease Of VAgal TonE in CHF [INOVATE-HF]; NCT01303718).
280                  The INOVATE-HF (Increase of Vagal Tone in Heart Failure) trial assessed the safety a
281 could mediate the neuromodulation of cardiac vagal tone in the rat model of HFpEF.
282                                      Cardiac vagal tone is a strong predictor of health, although its
283 ed whether respiratory modulation of cardiac vagal tone is intrinsically linked to post-inspiratory r
284 uency and tidal volume changes did not alter vagal tone or sympathetic activity).
285  suppressed RSA, whereas substantial cardiac vagal tone persisted.
286                     In control participants, vagal tone remained depressed during sustained hypoglyce
287 ers present reflex or persistent increase in vagal tone that may cause refractory symptoms even in a
288 horacic spinal pithing, cardiac chronotropic vagal tone was quantified by HR compared to its final le
289 tion of glucose in fasted mice activated the vagal tone without affecting blood pressure.
290 isms, such as alterations in parasympathetic vagal tone, did not appear to have a role in explaining
291  excess sympathetic activation and decreased vagal tone, is an integral component of the pathophysiol
292 ation with inflammation, fibrosis, increased vagal tone, slowed conduction velocity, prolonged cardio
293 ablished metric of HRV that reflects cardiac vagal tone.
294 ycemia at 1 h accompanied by reactivation of vagal tone.
295 ut, on average, only 52% of the chronotropic vagal tone.
296 xpedition, indicating a gradual reduction in vagal tone.
297 ucleus of the solitary tract further reduced vagal tone: remaining sources were untraced.
298 tal cortex activity, which in turn modulates vagal tone; a phenomenon associated with glucoregulation
299 cGMP and cAMP regulation of cardiac sympatho-vagal transmission in hypertension and ischaemic heart d
300                      Therefore, estimates of vagal villus afferent distributions (control minus VAGX)

 
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