ライフサイエンスコーパス: chemoreflex

1 ycardia and sympathoexcitation evoked by the chemoreflex.

2 flex and the slow component with the central chemoreflex.

3 pH as determinants of the ventilatory CO(2) chemoreflex.

4 pups showed no significant changes in anoxic chemoreflex.

5 ry responses to activation of the peripheral chemoreflex.

6 th muscle cells fully rescued the CO(2)/H(+) chemoreflex.

7 indicates an important role for the central chemoreflex.

8 virtually eliminates the central respiratory chemoreflex.

9 etic and respiratory responses of peripheral chemoreflex.

10 role for TRH signalling in the mammalian CO2 chemoreflex.

11 eathing and specifically the ventilatory CO2 chemoreflex.

12 effect on cardiorespiratory activity or the chemoreflex.

13 ripheral nervous systems associated with the chemoreflex.

14 contribute little to the central respiratory chemoreflex.

15 al pressure(MAP)with exaggerated sympathetic chemoreflexes.

16 o greatly compromised central and peripheral chemoreflexes.

17 CVR) arises from both peripheral and central chemoreflexes.

18 fetal heart rate (FHR), and fetal baro- and chemoreflexes.

19 uences NMDA receptor activation and arterial chemoreflexes.

20 reas to both TLR ligands blunted respiratory chemoreflexes.

21 tions of Kir5.1 to O(2)- and CO(2)-dependent chemoreflexes.

22 ed sympathetic nerve activity and peripheral chemoreflexes.

23 gon-like peptide-1) modulates the peripheral chemoreflex acting on the CB, supporting this organ as a

24 nitiation of sensory reflexes, including the chemoreflex activated during hypoxia.

25 lting in reduced ventilatory responsivess to chemoreflex activation by hypoxia and hypercapnia.

26 eptor-modulated ventilation, and ventilatory chemoreflex activation by hypoxia or hypercapnia.

27 bility that mechanisms other than peripheral chemoreflex activation contribute to vascular sympatheti

28 A exposure; mechanisms other than peripheral chemoreflex activation could be involved. Sherpa adaptat

29 respiratory muscle metaboreflex and arterial chemoreflex activation during exercise with blocked leg

30 respiratory muscle metaboreflex and arterial chemoreflex activation during FENT, subjects mimicked th

31 hemoreflexes are hyperactive in HFpEF and if chemoreflex activation exacerbates cardiac dysfunction a

32 Central chemoreflex activation had deleterious effects on cardia

33 ermine the effect of exercise-induced muscle chemoreflex activation on baroreflex sensitivity (BRS).

34 addition, the deleterious effects of central chemoreflex activation on cardiac autonomic balance and

35 Here, we reported that chemoreflex activation via electrical CSN stimulation, i

36 , the cardiovascular consequences of central chemoreflex activation were related to sympathoexcitatio

37 mpathetic responses induced by acute central chemoreflex activation.

38 but comparable ventilatory responsiveness to chemoreflex activation.

39 and deterioration of cardiac function during chemoreflex activation.

40 KEY POINTS: Enhanced carotid body chemoreflex activity contributes to development of disor

41 s study was to examine whether tonic carotid chemoreflex activity contributes to high resting and exe

42 Notably, acute attenuation of peripheral chemoreflex activity with hyperoxia did not restore card

43 2D; however, acute attenuation of peripheral chemoreflex activity with hyperoxia does not restore car

44 ccurred independently of changes in PASP and chemoreflex activity.

45 Tonic activation of excitatory chemoreflex afferents may contribute to increased effere

46 explained by tonic activation of excitatory chemoreflex afferents.

47 We conclude that, without the peripheral chemoreflex, AHCVR is adequately described by a single s

48 vasoconstrictor responses to hypoxaemia via chemoreflex and adrenomedullary actions.

49 mcg/kg/min) was used to inhibit the carotid chemoreflex and assess its tonic contribution to ventila

50 apping to measure the effects of baroreflex, chemoreflex and carbachol on pacemaker entrainment and e

51 ystolic pressure (PASP), peripheral arterial chemoreflex and high altitude-induced hypovolaemia are i

52 (i) An augmented CO2 chemoreflex and higher ABP in SHRs are measureable at a

53 in SHRs and contributes to the augmented CO2 chemoreflex and hypertension.

54 important role in the augmented central CO2 chemoreflex and in the development of hypertension in SH

55 We hypothesized that an augmented CO2 chemoreflex and overactive orexin system are linked with

56 n young SHRs and normalize the augmented CO2 chemoreflex and significantly lower the high ABP in adul

57 ROS in turn activate chemoreflex and suppress baroreflex, thereby stimulating

58 of the CB input to increase the gain of the chemoreflex and that caffeine abolishes CB acclimatizati

59 n acts in the carotid bodies (CB) to augment chemoreflex and that leptin activates the transient rece

60 poxia are triggered exclusively by a carotid chemoreflex and that they are modified by endocrine agen

61 hypoxaemia via actions involving the carotid chemoreflex and the adrenal medulla.

62 The augmented CO2 chemoreflex and the high ABP are measureable in young SH

63 in receptors can normalize the augmented CO2 chemoreflex and the high ABP in young SHRs and normalize

64 rapid component of AHCVR with the peripheral chemoreflex and the slow component with the central chem

65 vated neurons that contribute to the central chemoreflex and to breathing automaticity.

66 ory effect on breathing, they facilitate the chemoreflexes and a subset of them likely function as CO

67 depends on interactions between respiratory chemoreflexes and arousal state.

68 y response to CO2 has both rapid (peripheral chemoreflex) and slow (central chemoreflex) components.

69 the first integration site of the peripheral chemoreflex, and the nTS receives dense projections from

70 leus, which mediates the central respiratory chemoreflex; and the C1 neurons, which are hypoxia activ

71 This chemoreflex anti-inflammatory network was abrogated by c

72 The carotid chemoreflex appears to contribute to resting SBP in youn

73 The chemoreflexes are an important mechanism for regulation

74 Chemoreflexes are an important mechanism regulating both

75 Respiratory chemoreflexes are arousal state dependent whereas chemor

76 re, we tested whether peripheral and central chemoreflexes are hyperactive in HFpEF and if chemorefle

77 Ventilatory CO(2) and pH chemoreflexes are primarily determined by brain chemorec

78 cardiopulmonary reflex, baroreflexes and the chemoreflex, as well as other autonomic changes caused b

79 NFD), significantly blunted cardio/pulmonary chemoreflex bradycardic responses after 15 days, extendi

80 hyperoxia does not abolish the augmented CO2 chemoreflex (breathing and ABP) in SHRs, which indicates

81 itude and potentiate the central respiratory chemoreflex but do not appear to have a central respirat

82 -sensitive neurons contribute to the central chemoreflex but the number of candidates is high and gro

83 (iv) Attenuation of peripheral chemoreflexes by hyperoxia does not abolish the augmente

84 ular nucleus (PVN) contributes to peripheral chemoreflex cardiorespiratory responses, but specific PV

85 Increased carotid body chemoreflex (CBC) sensitivity plays a role in this proce

86 and impaired autoresuscitation during anoxic chemoreflex challenges.

87 showed that NO clamp treatment enhanced the chemoreflex component of the fetal cardiovascular defenc

88 d (peripheral chemoreflex) and slow (central chemoreflex) components.

89 emosensitivity, may possibly have peripheral chemoreflex contributions.

90 sought to determine if abnormal ventilatory chemoreflex control contributes to EX-inT in volume-over

91 ia OX(1)Rs in the region, to the hypercapnic chemoreflex control during wakefulness and to a lesser e

92 of restoring carotid body KLF2 expression on chemoreflex control of ventilation, sympathetic nerve ac

93 it is well accepted that altered peripheral chemoreflex control plays a role in the progression of h

94 volved with respiratory function and central chemoreflex control.

95 gh the exercise pressor reflex (EPR) and the chemoreflex (CR) are recognized for their sympathoexcita

96 ion of the muscle mechanoreflex (MMR) or the chemoreflex (CR) is different between men and women.

97 of the exercise pressor reflex (EPR) and the chemoreflex (CR) on the cardiovascular response to exerc

98 ion of the muscle mechanoreflex (MMR) or the chemoreflex (CR) was previously shown to be different be

99 ontrolled design, we examined the effects of chemoreflex deactivation (by comparing effects of breath

100 re (P=.02) were significantly reduced during chemoreflex deactivation by 100% oxygen only in patients

101 Animal studies suggest that chemoreflex defects are caused in part by the improper d

102 uring early life results in adult-onset O(2) chemoreflex deficiency.

103 ; P:=0.0001 and P:<0.0001, respectively) and chemoreflex delay (0.53+/-0.06 vs 0.40+/-0.06 and 0.30+/

104 ct responses to activation of the peripheral chemoreflex, diving response and arterial baroreflex, al

105 y, current evidence indicates the peripheral chemoreflex does not play a significant role in the augm

106 The CHF rats developed increased CB chemoreflex drive and chronic central pre-sympathetic ne

107 Increases in both peripheral and central chemoreflex drive are considered markers of the severity

108 Enhanced carotid chemoreflex drive from the CB is thought to contribute s

109 d sympathetic activity, and enhanced central chemoreflex drive has been shown in experimental and hum

110 denervation was performed to remove carotid chemoreflex drive in the CHF state (16 weeks post-myocar

111 Then, we hypothesized that the CB-mediated chemoreflex drive will be enhanced only in low output HF

112 Bursts share features of chemoreflex-driven clinical breathing patterns that also

113 s been substantial research/evidence linking chemoreflex dysfunction to cardiovascular illnesses such

114 Likewise, respiratory chemoreflexes evoked by changes in CO(2) or O(2) were un

115 B lowered its basal discharge and attenuated chemoreflex-evoked blood pressure and sympathetic respon

116 in attenuating the neuronal responses to the chemoreflex excitation and direct iontophoresis of N-met

117 xanthurenate, abolished resting activity and chemoreflex excitation of phrenic nerve activity, whilst

118 We conclude: (a) chemoreflex excitation of the phrenic nerves is mediated

119 The chemoreflex excitation of the two types of RVL respirato

120 hibition elicited by transient hyperoxia and chemoreflex excitation produced by exposure to graded, s

121 ition elicited by transient hyperoxia and to chemoreflex excitation produced by steady-state eucapnic

122 two groups of fetuses in FHR, MAP, baro- or chemoreflexes, femoral blood flow, femoral vascular resi

123 s the mechanisms underlying these responses, chemoreflex function and plasma concentrations of catech

124 recent evidence that peripheral and central chemoreflex function are altered in CHF and that they co

125 concentrations of noradrenaline and enhanced chemoreflex function during acute hypoxaemia.

126 vity of the CB chemoreceptors and peripheral chemoreflex function in CHF rabbits.

127 flow to the carotid body (CB) on peripheral chemoreflex function in rabbits.

128 We therefore tested the hypothesis that chemoreflex function is altered in CHF.

129 We tested the hypothesis that chemoreflex function is altered in patients with OSA.

130 Enhanced carotid body (CB) chemoreflex function is strongly related to cardiorespir

131 contrast, no studies to date have addressed chemoreflex function or its effect on cardiac function i

132 that both excitatory and inhibitory tests of chemoreflex function show congruence in the end-organ re

133 II) plays an important role in the enhanced chemoreflex function that occurs in congestive heart fai

134 atory-cardiovascular coupling (RCC), central chemoreflex function, cardiac autonomic control and card

135 eriod may contribute to the impaired central chemoreflex function.

136 A 100% increase in the chemoreflex gain (from 800 l min(-1) (fraction CO(2))(-1

137 The clinical data identify chemoreflex gain and delay time (rather than hyperventil

138 ons with the true determinants of stability: chemoreflex gain and mean CO(2).

139 hough our results support the idea that high chemoreflex gain destabilizes ventilatory control, there

140 70 +/- 0.083% (P < 0.0001), irrespective of chemoreflex gain or apnoea threshold.

141 DIO augments CB hypoxic chemoreflex gain via leptin.

142 Resting breathing variability, chemoreflex gain, cardiac function and sympatho-vagal ba

143 these oscillations to reveal the underlying chemoreflex hypersensitivity and reduced stability that

144 rotonergic neurons en masse blunts the CO(2) chemoreflex in adults, causing a difference in hypercapn

145 o effectively normalized the ventilatory CO2 chemoreflex in BN rats, but TAL did not affect CO2 sensi

146 xic sensing and the role of the carotid body chemoreflex in cardiorespiratory diseases.

147 in the reflex sensitivity of baroreflex and chemoreflex in in situ preparation.

148 The role of the carotid chemoreflex in maintaining high resting and exercise blo

149 emphasis has been placed on the role of the chemoreflex in mediating cardiopulmonary dysfunction dur

150 apezoid nucleus (RTN) attenuates the central chemoreflex in rats.

151 evidence implicates heightened carotid body chemoreflex in the progression of autonomic morbidities

152 st, almorexant, normalizes the augmented CO2 chemoreflex in young and adult SHRs and the high ABP in

153 These results suggest the carotid chemoreflex influences resting SBP in hypertensives but

154 ic, normocapnic perfusion), we found that CB chemoreflex inhibition decreased the slope of the ventil

155 entilatory and neurocirculatory responses to chemoreflex inhibition elicited by transient hyperoxia a

156 blood pressure and heart rate) responses to chemoreflex inhibition elicited by transient hyperoxia a

157 in resting systolic BP (SBP) during carotid chemoreflex inhibition in the HTN group.

158 there was a reduction in SBP during carotid chemoreflex inhibition with low-dose dopamine (2 mcg/kg/

159 cle exercise, SBP was reduced during carotid chemoreflex inhibition, but this was similar between gro

160 At rest, respiratory chemoreflexes initiated at peripheral and central sites

161 otrapezoid nucleus (RTN), a putative CRC and chemoreflex integrator.

162 are a critical component of the respiratory chemoreflex into adulthood.

163 Exaggerated hypoxic chemoreflex is a cardinal trait of SDB in obesity.

164 d oxygen concentration, and the carotid body chemoreflex is a major regulator of the sympathetic tone

165 The chemoreflex is a vital protective reflex that is crucial

166 The effect of leptin on CB hypoxic chemoreflex is completely abolished by a Trpm7 blocker F

167 We found that central chemoreflex is enhanced in HFpEF and neuronal activation

168 The present results show that the central chemoreflex is enhanced in HFpEF and that acute activati

169 The peripheral chemoreflex is known to be enhanced in individuals with

170 The peripheral chemoreflex is known to be hyper-responsive in both spon

171 in the setting of HF, potentiation of the CB chemoreflex is strongly associated with a reduction in c

172 leptin acts via TRPM7 in the CB to increase chemoreflex leading to SDB in obesity.

173 w summarizes recent advances in the study of chemoreflex malfunction and the underlying mechanisms in

174 Our data suggest that the peripheral chemoreflex may be a viable therapeutic target for renov

175 Our results suggest that the peripheral chemoreflex may be considered as a potential therapeutic

176 This facilitation of the chemoreflex may depend on the action of leptin in the hi

177 Abnormalities in chemoreflex mechanisms may be implicated in increased ca

178 glutamate and neuronal excitation augmented chemoreflex-mediated pressor, sympathoexcitatory and min

179 In the AM, sympathetic activation by the CB chemoreflex mediates CIH-induced HIF-alpha isoform imbal

180 exercise-induced alterations in respiratory chemoreflex might influence cerebral blood flow (CBF), i

181 lar nucleus (PVN) is essential to peripheral chemoreflex neurocircuitry, but the specific efferent pa

182 exercise-induced alterations in ventilatory chemoreflex on cerebrovascular CO(2) reactivity, these t

183 effect on resting breathing, blood gases or chemoreflexes (P >0.05).

184 r data showed that activation of the central chemoreflex pathway in HFpEF exacerbates diastolic dysfu

185 nic activation of the central and peripheral chemoreflex pathway plays a pivotal role in the pathophy

186 oform expression and oxidative stress in the chemoreflex pathway.

187 ted by hypoxia and facilitate the peripheral chemoreflex (PCR)-mediated hypoxic ventilatory response

188 tivity (MSNA) via activation of the arterial chemoreflex, pulmonary arterial baroreceptors and resett

189 ilatory oscillations generally result from a chemoreflex resonance, in which spontaneous biological v

190 baseline breathing or decreases the central chemoreflex, respectively, in mice during the light/inac

191 e the presence of upright CSR, assessment of chemoreflex response to hypoxia and hypercapnia, and 24-

192 eceptor-2 (PAR2) activation on the pulmonary chemoreflex responses and on the sensitivity of isolated

193 Dopamine inhibits chemoreflex responses during hypoxic breathing in normal

194 Ventilatory chemoreflex responses have been studied at rest during t

195 play a critical and differential role in the chemoreflex responses to hypoxia and hypercapnia.

196 from the PVN to the nTS is critical for full chemoreflex responses to hypoxia.

197 ht atrium immediately elicited the pulmonary chemoreflex responses, characterized by apnoea, bradycar

198 ly amplified the capsaicin-induced pulmonary chemoreflex responses.

199 This was because of differences in both chemoreflex sensitivity (1749+/-235 versus 620+/-103 and

200 Measurements, including chemoreflex sensitivity (S) and delay (delta), alveolar

201 We evaluated the relation between peripheral chemoreflex sensitivity and autonomic activity in patien

202 thermore, HFpEF rats showed increase central chemoreflex sensitivity but not peripheral chemosensitiv

203 c function in HF-EX-inT, and (ii) loss of CB chemoreflex sensitivity contributes to EX-inT in HF.

204 We observed elevated peripheral chemoreflex sensitivity in adults with diabetes which wa

205 od flow is the cause of increased peripheral chemoreflex sensitivity in CHF.

206 s involved in the augmentation of peripheral chemoreflex sensitivity in CHF.

207 d functional techniques assessing peripheral chemoreflex sensitivity in situ and in vivo.

208 activation of PAR2 upregulates the pulmonary chemoreflex sensitivity in vivo and the excitability of

209 d with sham rabbits, CAO enhanced peripheral chemoreflex sensitivity in vivo, increased CB chemorecep

210 Peripheral chemoreflex sensitivity is elevated in adults with T2D;

211 Peripheral chemoreflex sensitivity is potentiated in clinical and e

212 Chemoreflex sensitivity may be increased in patients wit

213 Average values for the chemoreflex sensitivity of the slow component of AHCVR d

214 Changes in peripheral chemoreflex sensitivity to CO2 in hypoxia correlated wit

215 The peripheral chemoreflex sensitivity to CO2 in hypoxia was reduced fr

216 We conclude that peripheral chemoreflex sensitivity to CO2 is reduced by somatostati

217 Central chemoreflex sensitivity to CO2 was unchanged.

218 her somatostatin also reduced the peripheral chemoreflex sensitivity to hypercapnia, and if so, wheth

219 lic acidosis, and that changes in peripheral chemoreflex sensitivity to hypoxia and acid are not impl

220 Despite reports of amplified carotid chemoreflex sensitivity to hypoxia in young adults with

221 t chemoreceptor afferents and hence decrease chemoreflex sensitivity to hypoxia.

222 Chemoreflex sensitivity was measured as the RSNA and min

223 id body decreased KLF2 expression, increased chemoreflex sensitivity, and increased AHI (6 +/- 2/h vs

224 Carotid chemoreflex sensitivity, assessed by the ventilatory res

225 istinguish the effect of isolated changes in chemoreflex sensitivity, mean F(ETCO(2)) and apnoeic thr

226 r and AT1-R antagonist reversed CAO-enhanced chemoreflex sensitivity.

227 F(ETCO(2)), high apnoeic thresholds or high chemoreflex sensitivity.

228 ously been shown to play a role in increased chemoreflex sensitivity.

229 ults with T2D exhibit exaggerated peripheral chemoreflex sensitivity; (2) the peripheral chemorecepto

230 ood flow associated with altered respiratory chemoreflex sensitivity; however, the mechanisms remain

231 mportantly, hyperglycemia-induced peripheral chemoreflex sensitization and associated basal sympathet

232 Peripheral chemoreflex sensitization is a feature of renovascular h

233 onditions like chronic intermittent hypoxia, chemoreflex sensitization may lead to respiratory disord

234 The chemoreflex stimulation as well as the surgical and phar

235 trol values (range 0-38%; n = 6), whereas CB chemoreflex stimulation increased the slope of the venti

236 By contrast, the chemoreflex stimulation increases the plasma levels of a

237 influence peak MAP responses to mechano- or chemoreflex stimulation of the hindlimb muscle.

238 -brainstem preparation during baroreflex and chemoreflex stimulation or with carbachol.

239 Chemoreflex stimulation produced similar effects but cen

240 sustained acidosis and the acute CO(2)/H(+) chemoreflex, suggesting plasticity within respiratory co

241 The chemoreflex sympathoexcitatory pressor responses were at

242 ity, these two subsystems of the respiratory chemoreflex system and cerebral CO(2) reactivity were ev

243 The respiratory chemoreflex system controlling ventilation consists of t

244 indings indicate that, despite an attenuated chemoreflex system controlling ventilation, elevations i

245 e rats (SHRs), resulting in an augmented CO2 chemoreflex that affects both breathing and ABP.

246 bably underlies the sleep apnoea and lack of chemoreflex that characterize congenital central hypoven

247 e (CNO) by systemic injection attenuated the chemoreflex that normally increases respiration in respo

248 1.1 in the afferent limb of the carotid body chemoreflex (the major regulator in the response to hypo

249 hemoreception theory' attributes the central chemoreflex (the stimulation of breathing by CNS acidifi

250 ast, whilst ANGII potentiated the peripheral chemoreflex, the NO donor was without effect.

251 eptor theory', endorsed here, attributes the chemoreflex to a limited number of specialized neurons.

252 ntifying the separate contributions of these chemoreflexes to AHCVR has been to associate the rapid c

253 e contribution of the peripheral and central chemoreflexes to augmented sympathetic discharge in CHF

254 to cause a severe attenuation of the central chemoreflex under anaesthesia.

255 ssing cells impaired RTN neurons, as well as chemoreflex under hypoxia and hypercapnia specially earl

256 de direct evidence that obesity increases CB chemoreflex via the leptin-Trpm7 pathway.

257 an ventilatory sensitivities for the central chemoreflex were (mean +/- s.e.m.) 1.69 +/- 0.39 l min-1

258 ventilatory sensitivities for the peripheral chemoreflex were 2.42 +/- 0.36 l min-1 Torr-1 in hypoxia

259 Hypoxia-induced chemoreflexes were examined by measuring integrated phre

260 tic station of afferents of baroreflexes and chemoreflexes, were evaluated using brainstem slices and

261 recognized role of 5-HT neurons in the CO(2) chemoreflex, whereby they enhance the response of the re

262 eptin deficiency causes an impairment of the chemoreflex, which can be reverted by leptin therapy.

263 ventilatory response of the respiratory CO2 chemoreflex, which normally augments ventilation in resp

264 late (hypoxic, normocapnic perfusate) the CB chemoreflex, while the systemic circulation, and therefo

265 ustained hypoxia (SH), activating peripheral chemoreflex with several autonomic and respiratory respo