ライフサイエンスコーパス: carotid body

1 d reduced nitric oxide (NO) signaling in the carotid body.

2 , is involved in the hypoxic response in the carotid body.

3 aling in mediating sensory plasticity of the carotid body.

4 s primarily localized to glomus cells of the carotid body.

5 hydroxylase and in the CSN axons within the carotid body.

6 sory neurons and their axons innervating the carotid body.

7 ased in several brain regions and within the carotid bodies.

8 rototypical Th2 cytokines also stimulate the carotid bodies.

9 s process are the pulmonary arteries and the carotid bodies.

10 k and by excitatory inputs, notably from the carotid bodies.

11 ains breathing despite the inactivity of the carotid bodies.

12 ssed in oxygen-sensitive glomus cells of the carotid body, a chemosensory organ at the carotid artery

13 r to be involved in chemotransmission of the carotid body, a major arterial chemoreceptor.

14 e, have been implicated in O2 sensing by the carotid body, a sensory organ that monitors arterial blo

15 We hypothesized that the carotid body, a tissue of neural crest origin, detect pa

16 roduce muscle vasodilatation, and stimulates carotid body A2 receptors to increase respiration.

17 onal approaches in early development include carotid body ablation and arteriovenous fistula placemen

18 operative assessment of the effectiveness of carotid body ablation, which has been recently proposed

19 emodynamic response was diminished following carotid body ablation.

20 In the CIH-conditioned animals, carotid body aconitase enzyme activity decreased compare

21 imulatory factors and cellular mechanisms of carotid body activation are unknown.

22 ects of hypoxia and AICAR on type I cell and carotid body activation.

23 s enzyme may offer a new target for reducing carotid body activity in selected cardiovascular disease

24 ear structurally intact, but hypoxia-induced carotid body activity is diminished.

25 quickly triggers a compensatory increase in carotid body activity.

26 ipitate hypoventilation and apnea, even when carotid body afferent input is normal.

27 y response is determined solely by increased carotid body afferent input to the brainstem.

28 We assessed rat carotid body afferent neural output in response to lower

29 Whether the low PO2 is detected at the carotid body, airway and/or the vasculature remains unkn

30 wn-regulation of HIF-2alpha was also seen in carotid bodies and adrenal medullae from IH-exposed rats

31 acid sensitivity, excitatory inputs from the carotid bodies and brain regions such as raphe and hypot

32 A rise in PCO(2) activates the carotid bodies and exerts additional effects on neurons

33 e verified P2X3 receptor expression in human carotid bodies and observed hyperactivity of carotid bod

34 ing on the circumstance, the activity of the carotid bodies and that of RTN vary in the same or the o

35 ibit exaggerated responses to hypoxia by the carotid body and adrenal chromaffin cells, which regulat

36 HIF-2 is critical for oxygen sensing by the carotid body and adrenal medulla, and for their control

37 hes the set point for hypoxic sensing by the carotid body and adrenal medulla, and is required for ma

38 Chemosensory reflexes initiated by the carotid body and catecholamine secretion from the adrena

39 Oxygen (O2) sensing by the carotid body and its chemosensory reflex is critical for

40 tudy, expression of TRPC proteins in the rat carotid body and petrosal ganglion was examined using im

41 pendent, oxygen-independent function for the carotid body and suggest that targeting PKCepsilon provi

42 Hypoxia increased SP release from the carotid body and the magnitude of release is dependent o

43 entral chemosensory transduction (within the carotid body and the medulla oblongata, respectively).

44 state, blunted oxygen sensing, and impaired carotid body and ventilatory responses to chronic hypoxi

45 bserved during hypoglycaemia by an augmented carotid body and whole body ventilatory CO2 sensitivity.

46 se in NOX activity in CIH but not in control carotid bodies, and this effect was associated with upre

47 on of atypical mitochondrial subunits in the carotid body, and genetic deletion of Cox4i2 mimicked th

48 sensory long-term facilitation (LTF) of the carotid body, and if so by what mechanism(s).

49 s and differences that exist between airway, carotid body, and pulmonary arteriolar O2 sensing.

50 tress, normalized hypoxic sensitivity of the carotid body, and restored autonomic functions in Hif-2a

51 an increase in the CO(2) sensitivity of the carotid body, and this effect is not due to the insulin-

52 We show that the carotid bodies are also sensitive to asthma-associated p

53 normalities present in diseases in which the carotid bodies are hyperactive at rest, e.g. essential h

54 c blood gas regulation, (2) suggest that the carotid bodies are not a major determinant of CO2 sensit

55 l and tissue studies have indicated that the carotid bodies are sensitive to glucose concentrations w

56 clusion, carotid sinus nerve inputs from the carotid body are, in part, responsible for elevated symp

57 our data support the notion of targeting the carotid body as a potential novel therapeutic approach f

58 , e.g., catecholamines are coreleased by the carotid body at hypercapnic, hypoxic and high-potassium

59 li induce extracellular ATP release from the carotid body at levels of 4-10 microM.

60 Lesions of the retrotrapezoid nucleus or carotid bodies attenuate, but do not eliminate, arousal

61 ecto-5'-nucleotidase (CD73) in vitro reduces carotid body basal discharge and responses to hypoxia an

62 se is consistent with a direct effect on the carotid body, but an indirect effect through the activat

63 Stimulation of the carotid bodies by these asthmakines involves a PKCepsilo

64 and ASIC3 were shown to be expressed in rat carotid body by quantitative PCR and immunohistochemistr

65 We showed that selective stimulation of the carotid body by the injection of adenosine into the caro

66 Isolated carotid body/carotid sinus nerve preparations were used

67 The carotid bodies (CB) are peripheral chemoreceptors that c

68 The carotid bodies (CB) express the long functional isoform

69 Clinical studies suggest that abnormal carotid body (CB) activity may be a driver of sleep apne

70 We denervated one carotid body (CB) and used extracorporeal blood perfusio

71 reased nitric oxide (NO) production enhanced carotid body (CB) chemoreceptor activity in chronic hear

72 In congestive heart failure (CHF), carotid body (CB) chemoreceptor activity is enhanced and

73 We asked if the type of carotid body (CB) chemoreceptor stimulus influenced the

74 nvestigate whether selective ablation of the carotid body (CB) chemoreceptors improves cardiorespirat

75 Enhanced carotid body (CB) chemoreflex function is strongly relat

76 SA), have been shown to exhibit a heightened carotid body (CB) chemosensory reflex and hypertension.

77 SA), have been shown to exhibit a heightened carotid body (CB) chemosensory reflex and hypertension.

78 a (IH) on blood pressure (BP), breathing and carotid body (CB) chemosensory reflex were examined in a

79 a (IH) on blood pressure (BP), breathing and carotid body (CB) chemosensory reflex were examined in a

80 The chemosensory glomus cells of the carotid body (CB) detect changes in O2 tension.

81 Carotid body (CB) glomus cells from rat express a TASK-l

82 Carotid body (CB) glomus cells mediate acute oxygen sens

83 t K(+) channels (Kv) are highly expressed in carotid body (CB) glomus cells, but their role in hypoxi

84 Augmented sensory neuronal activity from the carotid body (CB) has emerged as a principal cause of hy

85 To assess the contribution of the carotid body (CB) in observed ventilatory responses, CB

86 efficacy of intracerebral transplantation of carotid body (CB) in Parkinson's disease, possibly throu

87 scharge using an in vitro perfused adult rat carotid body (CB) in the presence and absence of these c

88 The carotid body (CB) is a major arterial chemoreceptor cont

89 The carotid body (CB) is a polymodal chemosensor of arterial

90 The carotid body (CB) is a polymodal sensor which increases

91 The carotid body (CB) is an arterial chemoreceptor organ loc

92 but the mechanism of this effect within the carotid body (CB) is not known.

93 of gene transcription, we hypothesized that carotid body (CB) neural activity contributes to CIH-ind

94 ect of chronically reduced blood flow to the carotid body (CB) on peripheral chemoreflex function in

95 The carotid body (CB) plays an important role in the control

96 Sustained hypoxia produces a carotid body (CB) sensitization, known as acclimatizatio

97 The view that the carotid body (CB) type I cells are direct physiological

98 sitive properties of glomus cells in the rat carotid body (CB) we used Ba2+, a non-specific inhibitor

99 ptin receptor, LepR(b) , was detected in the carotid body (CB), a key peripheral hypoxia sensor.

100 ceptor function and the actions of NO in the carotid body (CB), we compared the outward K+ currents (

101 chemosensory discharge was tested in the rat carotid body (CB).

102 principal peripheral chemoreceptors are the carotid bodies (CBs) and alteration in their function ha

103 Carotid bodies (CBs) are chemoreceptors that monitor and

104 ionally, we assessed the contribution of the carotid bodies (CBs), the main peripheral chemoreceptors

105 ly, by central chemoreceptors (CCRs) and the carotid bodies (CBs).

106 ) g(-1) in controls, P < 0.0001), as well as carotid body cell proliferation (400 +/- 81 vs. 2630 +/-

107 PHI induced only modest increases in HVR and carotid body cell proliferation, despite marked stimulat

108 ogating both ventilatory acclimatization and carotid body cell proliferative responses to sustained h

109 Furthermore, carotid body cells demonstrated HO-2-dependent hypoxic B

110 In vitro recordings of single carotid body chemoafferents showed that reducing superfu

111 The current model of O2 sensing by carotid body chemoreceptor (glomus) cells is that hypoxi

112 ery blood flow are associated with increased carotid body chemoreceptor activity.

113 Carotid body chemoreceptor function was examined by reco

114 on of peripheral and central chemoreception (carotid bodies, chemoreceptor afferents, chemoresponsive

115 contribute to chemotransduction of low pH by carotid body chemoreceptors and that extracellular acido

116 is intact, response gains physiological, and carotid body chemoreceptors are driven by a wide range o

117 We conclude that carotid body chemoreceptors in adult rats have responses

118 vagal afferents, whereas in wild-type mice, carotid body chemoreceptors played a predominant role.

119 Carotid body chemoreceptors respond to a decrease in art

120 Carotid body chemoreceptors sense hypoxemia, hypercapnia

121 at extracellular acidosis directly activates carotid body chemoreceptors through both ASIC and TASK c

122 the in situ responses in rats of single-unit carotid body chemoreceptors to changes in arterial PO2 a

123 We assessed the contribution of carotid body chemoreceptors to the ventilatory response

124 Increased carotid body chemoreflex (CBC) sensitivity plays a role

125 monstrated Kv1.1 in the afferent limb of the carotid body chemoreflex (the major regulator in the res

126 KEY POINTS: Enhanced carotid body chemoreflex activity contributes to develop

127 ences on hypoxic sensing and the role of the carotid body chemoreflex in cardiorespiratory diseases.

128 Emerging evidence implicates heightened carotid body chemoreflex in the progression of autonomic

129 Rat carotid body chemosensitive cells, and human neutrophils

130 In carotid body chemosensitive glomus cells, activation of

131 transmission is an important element of the carotid body chemotransduction pathway.

132 In CIH animals, carotid body complex I activity of the mitochondrial ele

133 We also show that the carotid bodies contribute predominantly to hypoxia-induc

134 s deficit could be due to an abnormally weak carotid body contribution to CO2 sensitivity.

135 Conversely, lentiviral KLF2 siRNA in the carotid body decreased KLF2 expression, increased chemor

136 Carotid body denervation (CBD) causes hypoventilation an

137 aminergic and inflammatory signaling during carotid body denervation-induced hypercapnia, we hypothe

138 s absent in healthy exercising animals after carotid body denervation.

139 Spontaneous Hypertensive (SH) rat carotid bodies display inherent hypersensitivity to hypo

140 However, release of SP from the carotid body during hypoxia has not been documented.

141 KEY POINTS: Carotid body dysfunction is recognized as a cause of hyp

142 H2S) is a physiologic gasotransmitter of the carotid body, enhancing its sensory response to hypoxia.

143 discharge in response to perturbation of the carotid body environment.

144 rived NECs were retained as PNECs, while the carotid body evolved via the aggregation of neural crest

145 Sensory activity was recorded from carotid bodies ex vivo.

146 ation-perfusion matching in the lung, whilst carotid body excitation by hypoxia initiates corrective

147 y underpin pulmonary artery constriction and carotid body excitation by hypoxia.

148 tion-perfusion matching in the lung, whereas carotid body excitation elicits corrective cardio-respir

149 Glomus cells, the site of O2 sensing in the carotid body, express cystathionine gamma-lyase (CSE), a

150 glomus) cells, the site of O2 sensing in the carotid body, express haem oxygenase-2 and cystathionine

151 vious application of fluorescent tracer onto carotid body for chemoreceptor afferents or onto aortic

152 n sinus nerve activity was recorded, whereas carotid bodies from Hif1a(+/-) mice responded to cyanide

153 Priming with H(2)O(2) elicited sLTF of carotid bodies from normoxic control rats and mice, simi

154 Experiments were performed on ex vivo carotid bodies from rats and mice exposed either to 10 d

155 g electrodes were placed at sites within the carotid body from which orthodromic APs could be evoked

156 ox regulation is required for maintenance of carotid body function and cardiorespiratory homeostasis.

157 ntilatory response to hypoxia depends on the carotid body function and sleep-wake states.

158 essengers in the sensory transduction at the carotid body, genetic and epigenetic influences on hypox

159 Carotid body glomus cells also expressed IL-1 receptor a

160 Isolated carotid body glomus cells also sense glucose, and animal

161 Carotid body glomus cells are the primary sites of chemo

162 Chemosensitive carotid body glomus cells exhibited toll-like receptor (

163 by measuring the pH sensitivity of isolated carotid body glomus cells from young spontaneously hyper

164 In carotid body glomus cells, AMPK is thought to link chang

165 that trigger amniote respiratory reflexes - carotid body glomus cells, and 'pulmonary neuroendocrine

166 be mediated by a drop in intracellular pH of carotid body glomus cells, which inhibits a K+ current.

167 myocytes and transmembrane Ca2+ influx into carotid body glomus cells.

168 t, it was targeted to the plasma membrane in carotid body glomus cells.

169 ed oxygen sensitivity of glomus cells in the carotid body has long puzzled physiologists.

170 BN rat carotid bodies have naturally higher CO and lower H2S le

171 and lower H2S levels than SD rat, whereas SH carotid bodies have reduced CO and greater H2S generatio

172 Reflexes from the carotid body have been implicated in cardiorespiratory d

173 anced ventilatory sensitivity to hypoxia and carotid body hyperplasia.

174 nd basal sympathetic activity and normalizes carotid body hyperreflexia in conscious rats with hypert

175 vivo adenoviral transfection of KLF2 to the carotid bodies in CHF rabbits restored KLF2 expression,

176 1) further support an important role for the carotid bodies in eupnoeic blood gas regulation, (2) sug

177 est therefore that any potential role of the carotid bodies in glucose homeostasis in vivo is mediate

178 carotid bodies and observed hyperactivity of carotid bodies in individuals with hypertension.

179 ion evoked initial sensory excitation of the carotid bodies in rats.

180 ion of sensory nerve discharge (sLTF) of the carotid body in rodents exposed to chronic intermittent

181 primary autonomic oxygen chemoreceptors, the carotid bodies, in parasympathetic-mediated asthmatic ai

182 glomus cells, isolated in clusters from rat carotid bodies, in response to hypoxia ( mmHg) and to ac

183 Reducing CO levels in BN rat carotid bodies increased H2S generation, restoring O2 se

184 n conclusion, down-regulation of KLF2 in the carotid body increases CBC sensitivity, oscillatory brea

185 atory pattern generator and persists without carotid body input.

186 Herein, we eliminated carotid body inputs in both PH-SHRs and SHRs to test the

187 are silent and the excitatory input from the carotid bodies is suppressed.

188 The carotid body is a sensory organ for detecting arterial b

189 The carotid body is an organ of the peripheral nervous syste

190 It is unclear whether the carotid body is directly stimulated by low glucose or by

191 This novel sensing role for the carotid body is mediated by a PKCepsilon-dependent stimu

192 When carotid bodies isolated from wild-type mice were exposed

193 ant in several mammalian tissues, and in the carotid body it is crucial to respiratory control.

194 We investigated the impact of restoring carotid body KLF2 expression on chemoreflex control of v

195 The results indicate that restoring carotid body KLF2 in chronic heart failure reduces sympa

196 apeutic approaches that increase KLF2 in the carotid bodies may be efficacious in the treatment of re

197 Recent evidence suggests that the carotid body may be one such site.

198 tudies have shown that reflexes arising from carotid bodies mediate CIH-evoked cardio-respiratory res

199 vation is critical for eliciting CIH-induced carotid body-mediated cardio-respiratory responses; (b)

200 low glucose, is an adequate stimulus for the carotid body-mediated changes in ventilation and CO2 sen

201 Concomitantly, hypoglycaemia evokes a carotid body-mediated hyperpnoea that maintains arterial

202 ates; and (2) behavioral characteristics and carotid body-mediated respiratory control during sleep w

203 Carotid body-mediated respiratory responses (decreased v

204 ine the intracellular signalling involved in carotid body-mediated sensing of asthmatic blood-borne i

205 ted with hypoxia-induced SP release from the carotid body, moderate level of hypoxia (12% O2+N2) was

206 ether D(1) receptors located centrally or on carotid bodies modulate these effects is not clear from

207 ological analysis revealed no differences in carotid body morphology between control and CIH animals.

208 ologic analysis revealed no abnormalities of carotid body morphology in Hif1a(+/-) mice.

209 For release studies, carotid bodies (n=56) were superfused with a modified Ty

210 -1 alpha deficiency has a dramatic effect on carotid body neural activity and ventilatory adaptation

211 To the extent that carotid body O(2) sensitivity is dependent on AMPK, our

212 ats, Brown-Norway (BN) rats exhibit impaired carotid body O2 sensing and develop pulmonary edema as a

213 Here, we report that inherent variations in carotid body O2 sensing by carbon monoxide (CO)-sensitiv

214 However, the carotid bodies of AMPK-knockout mice remained exquisitel

215 Expression of LepR(b) in the carotid bodies of LepR(b) deficient obese db/db mice inc

216 he peripheral arterial chemoreceptors in the carotid body of rats as a model system.

217 respiratory neurone channelopathy induced by carotid body overactivity in neurogenic hypertension tha

218 Importantly, carotid body oxygen sensing was unaffected by blocking e

219 As the carotid bodies' oxygen sensitivity is independent of PKC

220 Thirty-four patients underwent 41 primary carotid body paraganglioma resections (median follow-up

221 Carotid body paragangliomas are rare tumors that often a

222 ee survival after resection in patients with carotid body paragangliomas despite earlier intervention

223 Retrospective analysis of 34 patients with carotid body paragangliomas who underwent genetic testin

224 cal symptoms and tumor size in patients with carotid body paragangliomas.

225 xic hypocapnia, normocapnia and hypercapnia (carotid body PCO2 approximately 22, 41 and 68 mmHg, resp

226 nctional oxygen sensing: glomus cells of the carotid body (peripheral respiratory chemoreceptors) tha

227 the response to hypoxia), consisting of the carotid body, petrosal ganglion, and nucleus of the soli

228 tigated the possible molecular mechanisms of carotid body pH sensing by recording the responses of gl

229 e glucose, and animal studies have shown the carotid bodies play a role in the counterregulatory resp

230 esearch supports that over-activation of the carotid body plays a key role in metabolic diseases like

231 In an in vitro whole organ, rat carotid body preparation, CO increased sinus nerve chemo

232 nctional and/or structural plasticity in the carotid body, rats were subjected to 10 days of recurren

233 nd its current role in oxygen sensing by the carotid body; reactive oxygen species as key transducers

234 Increasing CO levels in SH carotid bodies reduced H2S generation, preventing hypers

235 Ch) is an excitatory neurotransmitter in the carotid body, regulating the excitability of afferent ne

236 ypoxia) oxygen-sensitive glomus cells of the carotid body release ATP to activate chemoafferent fibre

237 Hypoxia-evoked H2S generation in the carotid body requires the interaction of cystathionine-g

238 component of AHCVR was diminished following carotid body resection as has been suggested by studies

239 to describe AHCVR in patients with bilateral carotid body resections (BR) for glomus cell tumours.

240 These data support the idea that the carotid bodies respond to glucose and play a role in the

241 Glomus cells in the carotid body respond to decreases in oxygen tension of t

242 ic deletion of CSE display severely impaired carotid body response and ventilatory stimulation to hyp

243 uggest that developmental programming of the carotid body response to hypoxia involves epigenetic cha

244 Carotid body response to hypoxia was augmented, and acut

245 The carotid body's physiological role is to sense arterial o

246 Hypoxia-evoked H2S generation in the carotid body seems to require interaction of CSE with he

247 Chemoreceptors in the carotid bodies sense arterial oxygen tension and regulat

248 ated HIF-2alpha subunit results in augmented carotid body sensitivity to hypoxia, irregular breathing

249 poxia evoked long-term facilitation (LTF) of carotid body sensory activity in CIH-conditioned but not

250 endent, reversible, functional plasticity in carotid body sensory activity.

251 In vitro carotid body sensory discharge during hypoxia was greate

252 ur data show CD73 to be a novel regulator of carotid body sensory function and therefore suggest that

253 response to hypoxia is reflex in nature and carotid body sensory receptor constitutes the afferent l

254 Carotid bodies serve an essential role in this respect;

255 Confocal images through the carotid body showed that TRPC1/3/4/5/6 proteins localize

256 Supressing carotid body signalling through carotid sinus nerve (CSN

257 Pardal et al. now report the discovery of carotid body stem cells, which proliferate in response t

258 The carotid bodies stimulate the respiratory pattern generat

259 ine their response to chemoreceptor stimuli (carotid body stimulation and changes in brain pH) and to

260 f the acute respiratory response elicited by carotid body stimulation but contribute little to the ce

261 We have previously shown that carotid body stimulation by lysophosphatidic acid elicit

262 Finally, during hypocapnic hypoxia, carotid body stimulation increases breathing frequency v

263 into commNTS virtually blocked the effect of carotid body stimulation on SND in rats with intact caro

264 renergic neurons are vigorously activated by carotid body stimulation.

265 iate increase in ventilation is dependent on carotid body stimulation.

266 ited decreased D1 receptor protein levels in carotid bodies, striatum, and hypothalamic paraventricul

267 ls in glomus cells and sensory nerves of the carotid body suggests a role in facilitating and/or sust

268 characterizing the stimulus-response at rat carotid bodies superfused with high potassium concentrat

269 stance of approximately 100 microm above the carotid body surface for detecting extracellular ATP.

270 uantitative detection of ATP released at the carotid body surface in response to physiological stimul

271 Carotid bodies, the sensory organs for detecting arteria

272 Because TH-positive neurons project to the carotid body, this result suggests that TRPC1 is selecti

273 hypoxia-responsive respiratory network from carotid body to brainstem.

274 responses of glomus cells isolated from rat carotid body to rapid changes in extracellular pH using

275 present results showing a critical role for carotid body tonicity in the aetiology of enhanced centr

276 ra-2 AM to study the effects of hypoxia, and carotid body transmitters on intracellular calcium, [Ca2

277 omatic 74-year-old woman, on follow-up for a carotid body tumor, showed magnetic resonance imaging (M

278 Among 45 HNPs, 26 were carotid body tumors (CBTs), 15 glomus jugulare, 3 glomus

279 hich is mainly driven by higher frequency of carotid body tumors in patients with SDHD mutations.

280 a histochemical profile similar to mammalian carotid body Type I (glomus) cells and pulmonary neuroep

281 adult spontaneously hypertensive rats (SHRs) carotid body type I (glomus) cells exhibit hypersensitiv

282 derpinnings of the oxygen sensitivity of the carotid body Type I cells are becoming better defined as

283 d the CO2 sensitivity of freshly dissociated carotid body type I cells in vitro.

284 , cyanide (CN(-)) and oligomycin on isolated carotid body type I cells.

285 Background K-channels were abundant in carotid body type-1 cells from wild-type mice and compar

286 odest expansion of TH(+) glomus cells in the carotid body upon SDHC loss, PPGL is not observed in suc

287 plication of 5-HT elicits sensory LTF of the carotid body via activation of 5-HT(2) receptors, which

288 nformation that are both peripheral from the carotid bodies (via the nucleus of the solitary tract) a

289 Carotid body volume increased (0.0025 +/- 0.00017 in PHD

290 Estimates of carotid body volume were lower in aged hyperoxia-treated

291 The release of SP from superfused rabbit carotid body was determined by an enzyme immunoassay (EI

292 Glomus cells harvested from Wistar rat carotid bodies were cultured for 4 to 7 days.

293 lation blunted during hypoglycaemia when the carotid bodies were desensitized by hyperoxia.

294 nine, 4-chlorobenzenesulphonate) labeling of carotid bodies were obtained in a brain slice.

295 Carotid bodies were removed from anesthetized rats kept

296 prototypical acute O(2)-sensing organ is the carotid body, which contains glomus cells expressing K(+

297 ant components of the genetic make-up in the carotid body, which influence hypoxic sensing by regulat

298 s involvement in the hypoxic response in the carotid body, which involves interactions with a Ca(2+)-

299 his patient was found to have a tumor of the carotid body, which was likely a paraganglioma.

300 ng been known to be potent stimulants of the carotid body, yet their mechanism of action remains obsc