ライフサイエンスコーパス: vagal

1 the recent literature on the adrenergic and vagal abnormalities that have been reported in essential

2 ach compliance and induces early satiety via vagal actions.

3 Excessive compensatory vagal activation after the counterregulatory phase may a

4 e controls systemic inflammation by inducing vagal activation of aromatic L-amino acid decarboxylase,

5 es in reflexive and behavioural responses to vagal activation.

6 d post-inspiratory peaks in efferent cardiac vagal activity and suppressed RSA, whereas substantial c

7 Indirect measures of cardiac vagal activity are strongly associated with exercise cap

8 for selective modulation of sympathetic and vagal activity have recently been developed in an attemp

9 ncy component (0.15-0.4 Hz), an indicator of vagal activity, the low-frequency component (0.04-0.15 H

10 se in sympathetic activity and withdrawal of vagal activity.

11 ch NMDA receptor GluN2 subunits may regulate vagal afferent activity.

12 uinol in-2(1H)-yl)methanone; (CIQ)] enhanced vagal afferent calcium influx during stimulation.

13 re, we evaluated the contribution of central vagal afferent endings in MTII-induced reduction of food

14 nglion removal, resulting in degeneration of vagal afferent endings in the ipsilateral NTS, abolished

15 rallel and wrap around anterogradely labeled vagal afferent endings in the NTS and thus are aptly pos

16 ocortin-4 receptors (MC4Rs) are expressed by vagal afferent endings in the NTS, but it is not known w

17 )-catalyzed phosphorylation of synapsin I in vagal afferent endings, an effect known to increase syna

18 ave been many anterograde tracing studies of vagal afferent endings, but none on spinal afferent endi

19 brain MC4R activation is mediated by central vagal afferent endings.

20 ons show that astrocytes control presynaptic vagal afferent excitability directly under resting and a

21 nd GluN2D subunits may predominantly control vagal afferent excitability in the nucleus of the solita

22 via alterations in cAMP levels subsequent to vagal afferent fibre-dependent activation of metabotropi

23 nucleus of the solitary tract (NTS) receive vagal afferent innervations that initiate gastrointestin

24 TS and thus are aptly positioned to activate vagal afferent MC4Rs.

25 ity, these circadian fluctuations in gastric vagal afferent mechanosensitivity are lost.

26 ability of 5-HT to increase anterior gastric vagal afferent nerve (VAN) activity in vivo before and a

27 in cough is carried by the vagus nerve, and vagal afferent nerve terminals have been well defined in

28 that P2X3 receptors are expressed by airway vagal afferent nerves and contribute to the hypersensiti

29 t HFD does not alter the response of gastric vagal afferent nerves and neurones to 5-HT but attenuate

30 esponsible for symptoms and are regulated by vagal afferent nerves, which innervate the airway.

31 To test the hypothesis that vagal afferent neuron (VAN) GLP-1 receptors (GLP-1Rs) ar

32 y and function of 5-HT3 receptors on gastric vagal afferent neurones.

33 Vagal afferent neurons are therefore early integrators o

34 us determines the neurochemical phenotype of vagal afferent neurons by regulating a switch between st

35 Depending on the nutritional status, vagal afferent neurons express two different neurochemic

36 diet-induced obesity locks the phenotype of vagal afferent neurons in a state similar to that normal

37 The action of gut hormones on vagal afferent neurons is now recognised to be an early

38 eased in the inter-digestive period, inhibit vagal afferent neurons leading to increased food intake.

39 36); glucagon-like peptide-1 (GLP-1)) excite vagal afferent neurons to activate an ascending pathway

40 of calorie-rich diets reduces sensitivity of vagal afferent neurons to peripheral signals and their c

41 ctor, acting at type 1 receptors (CCK1Rs) on vagal afferent neurons; however, CCK agonists have faile

42 Patients with diabetes have defects in the vagal afferent pathway that result in abnormal gastroint

43 coming anorexigenic signals that act via the vagal afferent pathways.

44 addition to its role in ingestive behavior, vagal afferent signaling has been implicated modulating

45 rst evidence that diet-induced disruption to vagal afferent signaling may cause a perturbation in cir

46 These results suggest that glucose-dependent vagal afferent signalling is compromised by relatively s

47 This suggests that glucose-dependent vagal afferent signalling is compromised by short period

48 This disruption of vagal afferent signalling is sufficient to drive hyperph

49 c PAR1s modulate the activity of presynaptic vagal afferent terminals and postsynaptic neurons in the

50 yl-d-aspartate (NMDA) receptors expressed on vagal afferent terminals are involved in food intake and

51 oth postsynaptic NST neurons and presynaptic vagal afferent terminals.

52 ts mediate the NMDA receptor response on the vagal afferent terminals.

53 Gastric vagal afferents (GVAs) respond to mechanical stimuli to

54 urinary bladder and to assess whether those vagal afferents also innervate the colon.

55 bility and responsiveness of both peripheral vagal afferents and central vagal efferents but less inf

56 PV4 in mediating sensory nerve activation in vagal afferents and the possible downstream signaling me

57 The heterogeneity of vagal afferents and their central terminals within the N

58 Vagal afferents are an important neuronal component of t

59 Vagal afferents are involved in regulation of feeding be

60 be a consequence of increased activation of vagal afferents by pathology in the airways (e.g., infla

61 Vagal afferents exhibit a high probability of vesicle re

62 These studies clarify the roles of vagal afferents in mediating particular gut hormone resp

63 ity that glutamate release from unmyelinated vagal afferents may be regulated by a distinct, non-VGLU

64 der and colon and suggest that dichotomizing vagal afferents may provide a neural mechanism for cross

65 ences of complete disconnection of abdominal vagal afferents on innate anxiety, conditioned fear, and

66 Stimulation of vagal afferents or efferents in mice 24 hours before IRI

67 dent modulation of 5-HT responses in gastric vagal afferents prior to the development of obesity.

68 dent modulation of 5-HT responses in gastric vagal afferents prior to the development of obesity.

69 molecules into the CNS, and/or activation of vagal afferents that trigger CNS inflammation.

70 ot affect the response of gastric-projecting vagal afferents to 5-HT, it attenuates the ability of gl

71 ity attenuates the responsiveness of gastric vagal afferents to several neurohormones, the aim of the

72 used to identify distinct subpopulations of vagal afferents within NTS, we injected cholera toxin B

73 rt how primary visceral afferents, including vagal afferents, can maintain fidelity of transmission a

74 ted to visceral modulation through abdominal vagal afferents, possibly via changing limbic neurotrans

75 tory neurotransmitter released in the NTS by vagal afferents, which arrive there via the solitary tra

76 ibuted among the two distinct populations of vagal afferents.

77 mises the excitability and responsiveness of vagal afferents.

78 astric antrum/pylorus, enteric neurones, and vagal and dorsal root ganglia.

79 Some single vagal and spinal neurons provided dual innervation to bo

80 component (0.04-0.15 Hz), a mixture of both vagal and sympathetic activity, and the ratio of the low

81 This study tested the hypothesis that vagal and sympathetic control, as assessed by spectral a

82 e moment of lung inflation accounts for both vagal and sympathetic influences.

83 ted plasma corticosterone and increased both vagal and sympathetic nerve activity, C1-mediated IRI pr

84 duction properties and might be critical for vagal attenuation.

85 as found in both myelinated and unmyelinated vagal axons and terminals in medial NTS, whereas IB4 was

86 sympathetic nerve activity, cardiac sympatho-vagal balance and arrhythmia incidence in an animal mode

87 mia incidence, and improves cardiac sympatho-vagal balance and breathing stability.

88 ing molecules that modulate cardiac sympatho-vagal balance in the progression of heart disease.

89 moreflex gain, cardiac function and sympatho-vagal balance, and arrhythmia incidence were studied.

90 and spectral indicators of cardiac sympatho-vagal balance.

91 agal-sympathetic balance to a 4 : 1 sympatho-vagal balance.

92 Cardiac vagal baroreflex function was assessed using the modifie

93 agal metrics changed in opposite directions: vagal baroreflex gain and two indices of vagal fluctuati

94 agal metrics changed in opposite directions: vagal baroreflex gain and two indices of vagal fluctuati

95 ailed); altered arterial baroreceptor input (vagal baroreflex gain declined and muscle sympathetic ne

96 margin with at least 55% of patients in the vagal block group achieving a 20% loss and 45% achieving

97 ated to device, procedure, or therapy in the vagal block group was less than 15%.

98 cacy objectives, although weight loss in the vagal block group was statistically greater than in the

99 20 ng kg(-1) min(-1) (320 ADR), and (2) with vagal blockade (2 mg atropine), before and during intrav

100 Vagal blockade is proposed to inhibit aberrant orexigeni

101 Vagal blockade, which inhibits the vagus nerve, results

102 rising in obesity as a putative mechanism of vagal blockade-induced weight loss.

103 ress neuropeptide oxytocin (OXT) to modulate vagal brainstem circuits undergoes short-term plasticity

104 identify three novel subpopulations of EGFP+ vagal brainstem neurons: (a) EGFP+ neurons in the nAmb p

105 ration, recordings from the cut left cardiac vagal branch showed efferent activity that peaked in pos

106 In separate preparations with intact cardiac vagal branches but sympathetically denervated by thoraci

107 antagonist, ifenprodil, selectively reduced vagal calcium influx with stimulation compared to the ti

108 examine the modifications of sympathetic and vagal cardiovascular influences induced by current nonph

109 rs in the brain control heart activities and vagal cardiovascular reflexes involve purines.

110 or molecular GlyT1 knockdown, in the dorsal vagal complex (DVC) suppresses glucose production, incre

111 lso activates insulin receptor in the dorsal vagal complex (DVC) to lower glucose production through

112 Recent data highlight the dorsal vagal complex (DVC), lateral parabrachial nucleus (lPBN)

113 ve animals, OXT microinjection in the dorsal vagal complex induced a NO-mediated corpus relaxation.

114 in the subpallium, hypothalamus, and dorsal vagal complex of birds suggests that some of the functio

115 highly organized hypothalamic circuitry and vagal complex of nuclei to determine cessation of energy

116 way in rats, we placed tracers in the dorsal vagal complex or SNpc; brainstem and midbrain were exami

117 vation of dopamine 1 receptors in the dorsal vagal complex.

118 ation of nigro-vagal terminals in the dorsal vagal complex.

119 uctal gray, parabrachial nucleus, and dorsal vagal complex.

120 These findings indicate reduced vagal control and impaired cardiovascular homeostasis du

121 om the symptomatic MCs and from NMCs in less vagal control of heart rate and more reactive sympatheti

122 hetic control of the QT interval and reduced vagal control of heart rate are at lower risk.

123 The mechanisms underlying diminished vagal control of heart rate were investigated by studyin

124 Reduced cardiac vagal control reflected in low heart rate variability (H

125 ic pressure, other autonomic functions under vagal control.

126 ere, we used a rat model of subdiaphragmatic vagal deafferentation (SDA), the most complete and selec

127 ation (SDA), the most complete and selective vagal deafferentation method existing to date, to study

128 Vagal denervation was performed to assess its effect on

129 and critical atrial regions responsible for vagal denervation.

130 dback streams (auditory, proprioceptive, and vagal) did not alter the frequency or temporal precision

131 olished the post-inspiratory peak of cardiac vagal discharge (and cyclical HR modulation), although a

132 t experimental evidence that parasympathetic vagal drive generated by a defined CNS circuit determine

133 rmacological and morphological properties of vagal efferent motoneurones innervating the stomach.

134 both peripheral vagal afferents and central vagal efferents but less information is available regard

135 hrelin inhibition of leptin- or CCK-8-evoked vagal firing.

136 ns: vagal baroreflex gain and two indices of vagal fluctuations (root mean square of successive norma

137 ns: vagal baroreflex gain and two indices of vagal fluctuations rose and then fell in space, and desc

138 eriments showed that silencing Kir6.2 in the vagal ganglia abolished the orexigenic actions of ghreli

139 These neurons are found in the vagal ganglia and are characterized by the expression of

140 rising from the jugular (rather than nodose) vagal ganglia and the output of the Pa5 is predominately

141 These data indicate that ghrelin modulates vagal ganglia neuron excitability by activating KATP con

142 ns of ghrelin were abolished by treating the vagal ganglia neurons with pertussis toxin, as well as p

143 ghrelin were also abolished by treating the vagal ganglia neurons with pertussis toxin, as well as p

144 ulmonary C-fibers using a mouse ex vivo lung-vagal ganglia preparation.

145 dicating that Orai channel expression in the vagal ganglia was likely derived from non-neuronal cell

146 und Orai channel mRNA in extracts from whole vagal ganglia, but when using single cell RT-PCR analysi

147 vo vagus nerve and neuron cell bodies in the vagal ganglia.

148 nic laminar endings (IGLEs), the predominant vagal GI afferent, in mice with reduced intestinal BDNF

149 e alpha7 levels correlated directly with the vagal heart input and inversely with the magnitude of th

150 ological insight into heritable variation in vagal heart rhythm regulation, with a key role for genet

151 ates diastolic dysfunction, worsens sympatho-vagal imbalance and markedly increases the incidence of

152 HFpEF) display irregular breathing, sympatho-vagal imbalance, arrhythmias and diastolic dysfunction.

153 disordered breathing patterns, and sympatho-vagal imbalance.

154 rst confirm the presence of tonic inhibitory vagal influence on LV inotropy.

155 These results indicate that CRF alters vagal inhibitory circuits that uncover the ability of OX

156 verity of fibrosis in lungs with and without vagal innervation in unilaterally vagotomized mice.

157 Our results demonstrate evidence for vagal innervation of the bladder and colon and suggest t

158 rmine whether anatomical evidence exists for vagal innervation of the male rat urinary bladder and to

159 ta highlight and support the significance of vagal inputs and intestinal hormone peptides toward norm

160 le morphological information is available on vagal intramuscular arrays (IMAs), the afferents that in

161 lobe mainly ending medially to those of the vagal lobe, and those from the commissural nucleus ventr

162 descending projections to the SGN/V and the vagal lobe.

163 Main primary gustatory centers (facial and vagal lobes) received sensory projections from the facia

164 ephalon, thalamus, hypothalamus, facial, and vagal lobes, but substantially different in the dorsolat

165 la, and superficial layers of the facial and vagal lobes.

166 Vagal metrics changed in opposite directions: vagal baro

167 Vagal metrics changed in opposite directions: vagal baro

168 ircadian misalignment decreased wake cardiac vagal modulation by 8-15%, as determined by heart rate v

169 sinus arrhythmia (RSA), a measure of cardiac vagal modulation, provides cardiac risk stratification i

170 We identified and characterized a nigro-vagal monosynaptic pathway in rats that controls gastric

171 nges reflected by reciptocal sympathetic and vagal motoneurone responsiveness to breathing changes.

172 nd pharmacological responsiveness of central vagal motoneurones and that these changes were reversed

173 Immunohistochemical analyses of vagal motoneurones showed an increased number of oxytoci

174 ng their voltage-activated calcium channels, vagal motoneurons acquire a stressless form of pacemakin

175 to dopamine neurons in the substantia nigra, vagal motoneurons do not enhance their excitability and

176 I mGluRs similarly influence the response of vagal motoneurons to OXT.

177 rowth factor (HGF), by tissues innervated by vagal motor neurons during fetal development reveal pote

178 a suggest that MET+ neurons in the brainstem vagal motor nuclei are anatomically positioned to regula

179 ping of the viscerotopic organization of the vagal motor nuclei has provided insight into autonomic f

180 , trochlear, trigeminal motor, abducens, and vagal motor nuclei) contain protocadherin-19 and/or prot

181 c neurons residing in the brainstem's dorsal vagal motor nucleus dramatically impairs exercise capaci

182 The vagal nerve also projects to the commissural nucleus of

183 Collateral damage to the vagal nerve and the upper gastrointestinal (UGI) system

184 undred sixty-two patients received an active vagal nerve block device and 77 received a sham device.

185 weight loss was statistically greater in the vagal nerve block group (P = .002 for treatment differen

186 At 12 months, 52% of patients in the vagal nerve block group achieved 20% or more excess weig

187 In the intent-to-treat analysis, the vagal nerve block group had a mean 24.4% excess weight l

188 py-related serious adverse event rate in the vagal nerve block group was 3.7% (95% CI, 1.4%-7.9%), si

189 The adverse events more frequent in the vagal nerve block group were heartburn or dyspepsia and

190 ong patients with morbid obesity, the use of vagal nerve block therapy compared with a sham control d

191 acy objectives were to determine whether the vagal nerve block was superior in mean percentage excess

192 risk for subsequent PD, suggesting that the vagal nerve may be critically involved in the pathogenes

193 e enzymes in response to stimulation via the vagal nerve or the hormone cholecystokinin.

194 e) trial assessed the safety and efficacy of vagal nerve stimulation (VNS) among patients with HF and

195 Cervical vagal nerve stimulation (VNS) can improve left ventricul

196 Vagal nerve stimulation (VNS) is an alternative therapy

197 Vagal nerve stimulation (VNS) is well established.

198 es, in patients with depression or epilepsy, vagal nerve stimulation has been demonstrated to promote

199 though the mechanisms are poorly understood, vagal nerve stimulation prevents weight gain in response

200 high thoracic epidural anesthesia, low-level vagal nerve stimulation, and baroreflex stimulation.

201 ion, renal sympathetic denervation, cervical vagal nerve stimulation, baroreflex stimulation, cutaneo

202 Implantable cardiac vagal nerve stimulators are a promising treatment for ve

203 P2X2 -IR identifies probable vagal nerve terminals in the central (Ce) subnucleus in

204 opic pathogen entering the brain through the vagal nerve, a process that may take over 20 years.

205 iated by the injury to the components of the vagal nerve.

206 These findings indicate that vagal nerves that release several neurotransmitters may

207 ived sensory projections from the facial and vagal nerves, respectively.

208 During development, vagal neural crest cells fated to contribute to the ente

209 ebrates, a role that was largely subsumed by vagal neural crest cells in early gnathostomes.

210 m of jawed vertebrates arises primarily from vagal neural crest cells that migrate to the foregut and

211 ranscription factor meis3 is expressed along vagal neural crest pathways.

212 able regarding the effects of diet per se on vagal neurocircuit functions.

213 ulein-induced acute pancreatitis (AP) on the vagal neurocircuitry modulating pancreatic functions.

214 Vagal neurocircuits are vital to the regulation of upper

215 to a HFD modulates the processing of central vagal neurocircuits even in the absence of obesity.

216 rmacological and morphological properties of vagal neurocircuits regulating upper gastrointestinal tr

217 h fat diet (HFD) itself on the properties of vagal neurocircuits.

218 for the plausible effect of RYGB to improve vagal neuronal health in the brain by reversing some eff

219 of heart rate arises from pre-motor cardiac vagal neurons (CVNs) located in nucleus ambiguus (NA) an

220 influences brainstem parasympathetic cardiac vagal neurons (CVNs).

221 neurotransmission to parasympathetic cardiac vagal neurons in the rat nucleus ambiguus was determined

222 Enteric and vagal neurons positive for glp1r were activated by GLP-1

223 Patch clamp recordings of isolated rat vagal neurons show that ghrelin hyperpolarizes neurons b

224 In dissociated vagal neurons, antimycin A caused ROS-dependent PKC tran

225 and glycinergic inhibitory input to cardiac vagal neurons, with no significant effect on excitatory

226 arasympathetic output from brainstem cardiac vagal neurons.

227 travel provokes long-lasting sympathetic and vagal neuroplastic changes in healthy humans.

228 tify the pathway that connects the brainstem vagal nuclei and the SNpc, and to determine whether this

229 These changes with CIHH inhibit CVNs and vagal outflow to the heart, both in acute and chronic ex

230 serve as integrative targets for modulating vagal output activity to the stomach.

231 common were carotid paragangliomas (59) and vagal paragangliomas (27).

232 Carotid and vagal paragangliomas occurred most often.

233 at-induced model of Parkinsonism, this nigro-vagal pathway was compromised during the early stages of

234 ially engages the hypothalamus and brainstem vagal pathways in lean and obese women.

235 c nervous system, and effects of oxytocin on vagal pathways, as well as the antioxidant and anti-infl

236 ced inhibitory effect of Sst-GABA neurons on vagal pre-motor neurons in the DMV that control gastric

237 c control of LV contractility is provided by vagal preganglionic neurones located in the dorsal motor

238 eft ventricular contractility is provided by vagal preganglionic neurones of the dorsal motor nucleus

239 tional neuroanatomical mapping revealed that vagal preganglionic neurones that have an impact on left

240 ent of the left and right DVMN revealed that vagal preganglionic neurones, which have an impact on LV

241 The activity of the vagal preganglionic neurons is predominantly regulated b

242 ncing of the largest population of brainstem vagal preganglionic neurons residing in the brainstem's

243 (DMV) in the brainstem consists primarily of vagal preganglionic neurons that innervate postganglioni

244 e hindbrain is also the location of the vago-vagal reflex circuitry regulating gastric motility.

245 obesity, suggesting that attenuation of vago-vagal reflex signalling may precede the development of o

246 estinal motility, which are mediated by vago-vagal reflexes.

247 se neural crest leads to an altered sympatho-vagal regulation of cardiac rhythmicity in adults charac

248 GP ablation abated 100% of evoked vagal responses; these responses remained in 87% of cont

249 x; the anterior half receives input from the vagal-responsive and gustatory neurons in the basal part

250 ess is known about the mechanisms underlying vagal sensing itself.

251 e the inhibitory activity of theophylline on vagal sensory nerve activity and the cough reflex.

252 fect of theophylline on human and guinea pig vagal sensory nerve activity in vitro and on the cough r

253 nscious cough model in guinea pigs, isolated vagal sensory nerve and isolated airway neuron tissue- a

254 INT-BDNF(-/-) mice also exhibited increased vagal sensory neuron numbers, suggesting that their surv

255 e, we investigate the molecular diversity of vagal sensory neurons and their roles in sensing gastroi

256 Optogenetic activation of Piezo2(+) vagal sensory neurons causes apnoea in adult mice.

257 Within the gastrointestinal tract, vagal sensory neurons detect gut hormones and organ dist

258 Lastly, the role of vagal signaling or chewing gum as potential treatment st

259 and colon sensory innervation of spinal and vagal sources was determined.

260 mechanical responses to selective electrical vagal stimulation (EVS) were recorded from gastric fundu

261 We conclude that chronic vagal stimulation improves insulin sensitivity substanti

262 abolism, but the effect of chronic bilateral vagal stimulation is not known.

263 Acute vagal stimulation modifies glucose and insulin metabolis

264 ivities 12 weeks after permanent, bilateral, vagal stimulation performed at the abdominal level in ad

265 Vagal stimulation was associated with increased glucose

266 released from G-protein-coupled receptors on vagal stimulation.

267 his review examines the possibility of using vagal stimulators as a therapy for IBD.

268 ing workload-related transition from a 4 : 1 vagal-sympathetic balance to a 4 : 1 sympatho-vagal bala

269 We found that disruption of the vagal system in mice delayed resolution of Escherichia c

270 anoic acid (d,l-AP5) significantly inhibited vagal terminal calcium influx, while the excitatory amin

271 SNpc and/or optogenetic stimulation of nigro-vagal terminals in the dorsal vagal complex.

272 d capsaicin responses in isolated guinea pig vagal tissue, but glycopyrrolate and atropine did not.

273 cal antagonism is key to the transition from vagal to sympathetic dominance, and (iii) resetting of t

274 ime the influence of disinhibited eating and vagal tone (heart rate variability (HRV)) on hunger and

275 Substantial chronotropic vagal tone also remained after transection of the brains

276 responses is not clear, but an inhibition of vagal tone and a consequent reduction in mucus productio

277 sized that respiratory modulation of cardiac vagal tone and HR is intrinsically linked to the generat

278 Arterial pressure, vagal tone and muscle sympathetic outflow were comparabl

279 t-brainstem preparation shows strong cardiac vagal tone and pronounced respiratory sinus arrhythmia.

280 is associated with reduced baseline cardiac vagal tone and that this reduction correlates with left-

281 normogastria/tachygastria ratio and cardiac vagal tone but higher cardiac sympathetic index in compa

282 We conclude that cardiac vagal tone depends on neurons in at least three sites of

283 We conclude that cardiac vagal tone depends upon at least 3 sites of the pontomed

284 Respiratory-linked fluctuations in cardiac vagal tone give rise to respiratory sinus arryhthmia (RS

285 (INcrease Of VAgal TonE in CHF [INOVATE-HF]; NCT01303718).

286 The INOVATE-HF (Increase of Vagal Tone in Heart Failure) trial assessed the safety a

287 Cardiac vagal tone is a strong predictor of health, although its

288 ed whether respiratory modulation of cardiac vagal tone is intrinsically linked to post-inspiratory r

289 uency and tidal volume changes did not alter vagal tone or sympathetic activity).

290 suppressed RSA, whereas substantial cardiac vagal tone persisted.

291 In control participants, vagal tone remained depressed during sustained hypoglyce

292 horacic spinal pithing, cardiac chronotropic vagal tone was quantified by HR compared to its final le

293 isms, such as alterations in parasympathetic vagal tone, did not appear to have a role in explaining

294 excess sympathetic activation and decreased vagal tone, is an integral component of the pathophysiol

295 ation with inflammation, fibrosis, increased vagal tone, slowed conduction velocity, prolonged cardio

296 ycemia at 1 h accompanied by reactivation of vagal tone.

297 ut, on average, only 52% of the chronotropic vagal tone.

298 ucleus of the solitary tract further reduced vagal tone: remaining sources were untraced.

299 tal cortex activity, which in turn modulates vagal tone; a phenomenon associated with glucoregulation

300 cGMP and cAMP regulation of cardiac sympatho-vagal transmission in hypertension and ischaemic heart d