ライフサイエンスコーパス: chemoreflex

1 ry responses to activation of the peripheral chemoreflex.

2 ycardia and sympathoexcitation evoked by the chemoreflex.

3 flex and the slow component with the central chemoreflex.

4 indicates an important role for the central chemoreflex.

5 virtually eliminates the central respiratory chemoreflex.

6 etic and respiratory responses of peripheral chemoreflex.

7 role for TRH signalling in the mammalian CO2 chemoreflex.

8 eathing and specifically the ventilatory CO2 chemoreflex.

9 effect on cardiorespiratory activity or the chemoreflex.

10 ripheral nervous systems associated with the chemoreflex.

11 contribute little to the central respiratory chemoreflex.

12 o greatly compromised central and peripheral chemoreflexes.

13 CVR) arises from both peripheral and central chemoreflexes.

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

15 uences NMDA receptor activation and arterial chemoreflexes.

16 ed sympathetic nerve activity and peripheral chemoreflexes.

17 al pressure(MAP)with exaggerated sympathetic chemoreflexes.

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

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

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

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

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

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

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

25 but comparable ventilatory responsiveness to chemoreflex activation.

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

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

28 explained by tonic activation of excitatory chemoreflex afferents.

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

30 vasoconstrictor responses to hypoxaemia via chemoreflex and adrenomedullary actions.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

45 This chemoreflex anti-inflammatory network was abrogated by c

46 The chemoreflexes are an important mechanism for regulation

47 Chemoreflexes are an important mechanism regulating both

48 Respiratory chemoreflexes are arousal state dependent whereas chemor

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

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

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

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

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

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

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

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

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

58 emosensitivity, may possibly have peripheral chemoreflex contributions.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

74 The chemoreflex excitation of the two types of RVL respirato

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

90 70 +/- 0.083% (P < 0.0001), irrespective of chemoreflex gain or apnoea threshold.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

112 Abnormalities in chemoreflex mechanisms may be implicated in increased ca

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

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

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

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

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

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

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

120 oform expression and oxidative stress in the chemoreflex pathway.

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

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

123 Dopamine inhibits chemoreflex responses during hypoxic breathing in normal

124 Ventilatory chemoreflex responses have been studied at rest during t

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

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

127 ly amplified the capsaicin-induced pulmonary chemoreflex responses.

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

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

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

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

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

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

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

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

136 Peripheral chemoreflex sensitivity is potentiated in clinical and e

137 Chemoreflex sensitivity may be increased in patients wit

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

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

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

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

142 Central chemoreflex sensitivity to CO2 was unchanged.

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

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

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

146 Chemoreflex sensitivity was measured as the RSNA and min

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

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

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

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

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

152 Peripheral chemoreflex sensitization is a feature of renovascular h

153 The chemoreflex stimulation as well as the surgical and phar

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

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

156 The chemoreflex sympathoexcitatory pressor responses were at

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

158 The respiratory chemoreflex system controlling ventilation consists of t

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

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

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

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

163 1.1 in the afferent limb of the carotid body chemoreflex (the major regulator in the response to hypo

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

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

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

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

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

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

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

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

172 Hypoxia-induced chemoreflexes were examined by measuring integrated phre

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

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

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

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

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

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