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 pothesis of O(2) chemoreception in the whole carotid body.

8 production, is not the oxygen sensor in mice carotid body.

9 ptors and D(2)-dopamine receptors in the rat carotid body.

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

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

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

13 ains breathing despite the inactivity of the carotid bodies.

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

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

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

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

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

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

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

21 emodynamic response was diminished following carotid body ablation.

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

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

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

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

26 quickly triggers a compensatory increase in carotid body activity.

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

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

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

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

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

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

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

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

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

36 The carotid bodies and their associated nerves were removed

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

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

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

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

41 ermined whether hypoxia releases SP from the carotid body and further characterized the mechanism(s)

42 udies indicated that SP is excitatory to the carotid body and is associated with sensory response to

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

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

45 cted A(2a)-adenosine receptor protein in the carotid body and petrosal ganglion.

46 ipheral chemoreceptors (glomus cells) in the carotid body and relay neurons in the nucleus of the sol

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

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

49 ons between cultured glomus cells of the rat carotid body and to assess the effects of acidity and ac

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

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

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

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

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

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

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

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

58 he aim of this study was to determine if the carotid bodies are involved in basal glucoregulation or

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

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

61 The carotid bodies are sensitive to glucose in vitro and can

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

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

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

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

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

67 were perfused with blood, stimulation of the carotid bodies being carried out by three different leve

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

69 suggest that SP is released from the rabbit carotid body by hypoxia that depends on the severity of

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

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

72 Isolated carotid body/carotid sinus nerve preparations were used

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

103 The most common tumor site is the carotid body (CB), a chemoreceptive organ that senses ox

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

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

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

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

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

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

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

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

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

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

114 Carotid body chemoreceptor function was examined by reco

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

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

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

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

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

120 Carotid body chemoreceptors respond to a decrease in art

121 Carotid body chemoreceptors sense hypoxemia, hypercapnia

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

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

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

125 e to increasing levels of stimulation of the carotid body chemoreceptors, together with an examinatio

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

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

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

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

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

131 Rat carotid body chemosensitive cells, and human neutrophils

132 In carotid body chemosensitive glomus cells, activation of

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

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

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

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

137 Carotid body denervation (CBD) causes hypoventilation an

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 Carotid bodies from diverse species contain substance P

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

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

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

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

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

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

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

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

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

162 Carotid body glomus cells are the primary sites of chemo

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

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

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

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

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

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

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

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

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

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

184 atory pattern generator and persists without carotid body input.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

201 Carotid body-mediated respiratory responses (decreased v

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

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

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

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

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

207 -1 alpha deficiency has a dramatic effect on carotid body neural activity and ventilatory adaptation

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

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

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

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

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

213 In conclusion, we found that the carotid bodies (or receptors anatomically close by) play

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

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

216 Carotid body paragangliomas are rare tumors that often a

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

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

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

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

221 ts were additive, at least for PO2 levels of carotid body perfusate down to approximately 40 mmHg.

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

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

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

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

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

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

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

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

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

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

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

233 es and their associated nerves were removed (carotid body resected [CBR]) or left intact (Sham), and

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

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

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

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

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

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

240 Carotid body response to hypoxia was augmented, and acut

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

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

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

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

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

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

247 In vitro carotid body sensory discharge during hypoxia was greate

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

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

250 Carotid bodies serve an essential role in this respect;

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

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

253 The carotid bodies stimulate the respiratory pattern generat

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

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

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

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

258 renergic neurons are vigorously activated by carotid body stimulation.

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

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

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

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

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

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

265 Carotid bodies, the sensory organs for detecting arteria

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

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

268 of peripheral arterial chemoreceptors in the carotid body to hypoxia increases with postnatal maturat

269 acellular calcium ([Ca(2+)](i)) responses of carotid body to hypoxia.

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

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

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

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

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

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

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

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

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

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

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

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

282 and acid-sensitive background K+ channel of carotid body type-I cells is likely to be an endogenous

283 xygen-sensitive background K+ current in rat carotid body type-I cells were investigated and compared

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

285 The estimated carotid body volume in control rats (11.5 (+/- 0.7) x 10

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

287 However, carotid body volume was significantly greater in hyperox

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

289 Removal of carotid bodies was verified by the absence of a ventilat

290 rs and the concentration of SP in the rabbit carotid body was 1.5+/-0.1 ng/mg protein.

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 regulated in presumably type I cells in the carotid body which may contribute to the maturation of h

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