ライフサイエンスコーパス: baroreceptor

1 innervating the aortic arch to function as a baroreceptor.

2 of KCNQ2, KCNQ3 and KCNQ5 channels in aortic baroreceptors.

3 he M-current to the function of the arterial baroreceptors.

4 acteristics expected from pulmonary arterial baroreceptors.

5 ovascular responses to unloading the carotid baroreceptors.

6 hat receive the densest inputs from arterial baroreceptors.

7 onergic cell discharge through activation of baroreceptors.

8 concomitant stimulation of coronary arterial baroreceptors.

9 ondary to loading/unloading of carotid sinus baroreceptors.

10 rgent excitation of the neurones by arterial baroreceptors.

11 ecies suppress action potential discharge of baroreceptors.

12 GABAergic inhibition of VP neurons by aortic baroreceptors.

13 body chemoreceptors (81 %) but not arterial baroreceptors (3 %; i.e. n = 1 neurone), whereas distens

14 tive cells (n = 13) were activated mainly by baroreceptors (86 %) rather than peripheral chemorecepto

15 diorespiratory receptors (primarily arterial baroreceptors) accounted for 37 % of the total substance

16 b) 2/159 (1%) convergent cells responding to baroreceptor activation and light touch; (c) 44/159 (28%

17 alamus blocked the right insular response to baroreceptor activation by >70%.

18 erotonergic cell responses to all methods of baroreceptor activation were small in magnitude and were

19 erhemispheric connectivity also responded to baroreceptor activation, further emphasizing the connect

20 Rhythmic feedback of cardiac and baroreceptor activity contributes dynamically to homeost

21 Multiple measures of baroreceptor activity each suggest that mechanosensitivi

22 rhythm in SND involves a direct influence of baroreceptor activity on the 10-Hz oscillator.

23 ted synchrony confined to periods of altered baroreceptor activity were detected and involved neurone

24 rial blood pressure signal which represented baroreceptor activity.

25 f serotonergic cells in RM are influenced by baroreceptor activity.

26 Any influence of baroreceptor afferent activity on ordinary spectra of ce

27 re occurs, the information is transmitted by baroreceptor afferent fibers to the central network by g

28 The primary baroreceptor afferent fibres make their first excitatory

29 entification of weapons during systole, when baroreceptor afferent firing is maximal, relative to dia

30 nduced by i.v. infusion of phenylephrine, or baroreceptor afferent inactivation, caused by carotid ar

31 e-related differences in the distribution of baroreceptor afferent information to brainstem sympathet

32 mpathetic-related neurons receive peripheral baroreceptor afferent input, but are not interconnected,

33 the relationship between nerve activity and baroreceptor afferent input.

34 release from the rostral NTS in response to baroreceptor afferent input.

35 subtypes are involved in the integration of baroreceptor afferent inputs within the nucleus of the s

36 which EAA receptor subtypes are involved in baroreceptor afferent integration by second and higher o

37 ionotropic EAA receptor subtypes involved in baroreceptor afferent integration in the NTS.

38 ed phase locking of SND to pulse-synchronous baroreceptor afferent nerve activity.

39 of fear and threat and counter the view that baroreceptor afferent signaling is always inhibitory to

40 an important neurotransmitter released from baroreceptor afferent synapses in the NTS, the influence

41 on glutamate a major neurotransmitter at the baroreceptor afferent terminals inhibits its own release

42 s long been appreciated as a primary site of baroreceptor afferent termination in the central nervous

43 after PE injection, and sections through the baroreceptor afferent zone of the NTS prepared for preem

44 in a circumscribed, rostral, portion of the baroreceptor afferent zone of the NTS, whereas only a sm

45 (NTS) to the termination patterns of primary baroreceptor afferents and in the caudal ventrolateral m

46 medulla, the NTS is the termination site of baroreceptor afferents and is essential for mediating th

47 Synaptic transmission between baroreceptor afferents and the nucleus tractus solitariu

48 ortic nerve, a nerve that contains primarily baroreceptor afferents from the aortic arch.

49 isometric muscle contraction, activation of baroreceptor afferents induced by i.v. infusion of pheny

50 is the first site of integration for primary baroreceptor afferents, which release glutamate to excit

51 y into the NTS at the site of termination of baroreceptor afferents.

52 sence of anterograde tracers from peripheral baroreceptor afferents.

53 afferents or onto aortic depressor nerve for baroreceptor afferents.

54 transmitter contained in first-order sensory baroreceptor afferents; however, ultrastructural support

55 urves were obtained for carotid and coronary baroreceptors after maintaining the distending pressure

56 of-principle trial with a novel endovascular baroreceptor amplification device, MobiusHD (Vascular Dy

57 ts with resistant hypertension, endovascular baroreceptor amplification with the MobiusHD device subs

58 ose areas modified by oestrogen's action and baroreceptor and chemoreceptor denervation.

59 tradiol augments the activity of the central baroreceptor and chemoreceptor reflex pathways, and that

60 test the effect of oestradiol on the central baroreceptor and chemoreceptor reflex pathways.

61 Heart morphology, blood pressure, baroreceptor and HPA function were assessed in male F(1)

62 Neurons convergent for baroreceptor and nociceptive input have also been identi

63 nucleus of the solitary tract (NTS) on both baroreceptor and peripheral chemoreceptor reflexes was c

64 that the known excitatory effect of PGI2 on baroreceptor and vagal afferent fibres is mediated by in

65 h arises from alterations to both peripheral baroreceptors and central autonomic nuclei such as the n

66 The specific convergence pattern of baroreceptors and chemoreceptors to these cardioreceptiv

67 est that astrocytes function as intracranial baroreceptors and play an important role in homeostatic

68 This study expands the molecular profiles of baroreceptors and provides new insights into molecular m

69 ation of MSNA and suggest that feedback from baroreceptors and pulmonary stretch receptors are the do

70 sed the threshold for activation of arterial baroreceptors and shifted the pressure-response curve to

71 y opposite polysynaptic inputs from arterial baroreceptors and trigeminal afferents.

72 iple traits (CHGB, catecholamines, autonomic/baroreceptor, and renal function), including several fea

73 harge is restrained continuously by arterial baroreceptors, and C1 neuron activation is critical to s

74 ultrasonography at the level of the arterial baroreceptors, and MSNA via microneurography were contin

75 cing capacity) of an elastic artery in which baroreceptors are located is associated with these age-e

76 Arterial baroreceptors are mechanosensitive nerve endings in the

77 diastole, the period between heartbeats when baroreceptors are quiescent.

78 To function as intracranial baroreceptors, astrocytes must possess a specialized mem

79 t of stimuli to arterial and cardiopulmonary baroreceptors by increasing cardiac filling pressures an

80 These carotid baroreceptors can be stimulated non-invasively by extern

81 ucleus tractus solitarii (NTS) depressed the baroreceptor cardiac reflex.

82 Simulated microgravity impairs vagal baroreceptor-cardiac reflex function and causes orthosta

83 Baroreceptor-cardiac reflex relations were displaced dow

84 pressure (BP) responses to selective carotid baroreceptor (CBR) unloading and loading in 14 young (22

85 A model for catestatin action in the baroreceptor center of the nucleus of the tractus solita

86 cally, monosynaptic projections from primary baroreceptor centers to the LC have been suggested by el

87 opic glutamate autoreceptors (mGluRs) on the baroreceptor central terminals to suppress its further r

88 Insular neurons responsive to baroreceptor challenge have been identified in the rat,

89 s regions based on afferent information from baroreceptors, chemoreceptors, nociceptors, and circulat

90 ar tachyarrhythmias and that cardiopulmonary baroreceptors contribute significant inhibitory modulati

91 lar rhythms derived from intrinsic delays in baroreceptor control, and experimental evidence subseque

92 ischarge, its vasoconstrictor effect and its baroreceptor control, during pregnancy and postpartum in

93 tic nerve activity (SNA), which is not under baroreceptor control.

94 etions were significantly heritable, as were baroreceptor coupling (heart rate response to BP fluctua

95 d NO excretion, as well as autonomic traits: baroreceptor coupling, maximum pulse interval, and pulse

96 ibutes greatly to the hypertension caused by baroreceptor deafferentation.

97 In baroreceptor denervated and vagotomized cats, the presen

98 ythm in sympathetic nerve discharge (SND) of baroreceptor-denervated, urethane-anesthetized cats.

99 ill reduced heart rate in dogs with arterial baroreceptor denervation, but not after ganglionic block

100 oherence analysis and by their absence after baroreceptor denervation.

101 Baroreceptor discharge at ventricular systole underpins

102 ioration may be a consequence of cardiac and baroreceptor dysfunction or may be primarily caused by i

103 equired to assess the effect of differential baroreceptor feedback (i.e. aortic-carotid g-gradient).

104 develop a modeling framework for predicting baroreceptor firing rate as a function of blood pressure

105 gulation of cardiovascular functions through baroreceptor function.

106 alt intake and heart rate, indicating intact baroreceptor function.

107 ar lesions, however, significantly increased baroreceptor gain (p<0.0001) whereas right posterior ins

108 t posterior insular lesions had no effect on baroreceptor gain although heart rate and blood pressure

109 In this study, baroreceptor gain was investigated in response to the sy

110 were virtually abolished, DA did not modify baroreceptor gain.

111 nt cortex were without significant effect on baroreceptor gain.

112 Both carotid and aortic arch baroreceptors have been shown to reset after as little a

113 the involvement of nitric oxide (NO) in the baroreceptor-heart rate reflex pathway.

114 ve tonic excitatory inputs from the arterial baroreceptors; however, these tonic inputs appear to be

115 AV3V region increase the sensitivity of the baroreceptor HR reflex in conscious rats.

116 li to either the arterial or cardiopulmonary baroreceptors in 9 patients.

117 lective pressure activation of carotid sinus baroreceptors in an isolated sinus or selective denervat

118 lative roles of cardiopulmonary and arterial baroreceptors in controlling SNA and arterial pressure d

119 tion occurring in response to stimulation of baroreceptors in the aortic arch, carotid sinuses and co

120 fferent cardiovascular signals from arterial baroreceptors in the carotid sinuses are processed withi

121 sed animal model, independent stimulation of baroreceptors in the pulmonary artery elicits reflex sym

122 Mechanical stretch of baroreceptors in the wall of the aortic arch and carotid

123 espiratory receptors (predominantly arterial baroreceptors) increases the extraneuronal concentration

124 rotid baroreceptors or denervation of aortic baroreceptors, indicating no convergence of activity fro

125 ight integration of somatosensory and phasic baroreceptor information at cortical, limbic and brainst

126 e show that chronic high salt intake impairs baroreceptor inhibition of rat VP neurons through a brai

127 When baroreceptor innervation (aortic depressor amd carotid s

128 Moreover, baroreceptor innervation is absent in newborn mice lacki

129 nses to cardiac-related afferent inputs when baroreceptor innervation is intact.

130 coherent rhythm was found in 7/34 units when baroreceptor innervation was intact, where it co-existed

131 ity (hypocapnia prevailed); altered arterial baroreceptor input (vagal baroreflex gain declined and m

132 rves were dependent upon peripheral afferent baroreceptor input in most animals.

133 ections; and (c) a significant proportion of baroreceptor input relays to the posterior insula throug

134 first station in the processing of arterial baroreceptor input, and their responses to stimulation.

135 s in the medullary raphe magnus (RM) receive baroreceptor input, cells were tested for their response

136 nd in the absence of changes in the arterial baroreceptor input, the primary cardio-inhibitory and va

137 ons excites an inhibitory pathway modulating baroreceptor input, thus contributing to the increase in

138 stent with these CVPNs receiving an arterial baroreceptor input.

139 ythms, is modulated by the level of arterial baroreceptor input.

140 ect effect of reducing MAP and thus arterial baroreceptor input.

141 vagal tone were achieved by altering carotid baroreceptor input: neck pressure (NP) or neck suction (

142 nal cord and that are modulated by different baroreceptor inputs are considered the main central gene

143 ng changes in arterial pressure suggest that baroreceptor inputs are integrated differently in MSNs c

144 urations than those to PSNs, suggesting that baroreceptor inputs to MSNs and PSNs are mediated by dif

145 th normal breathing, activity from pulmonary baroreceptors is obtained at physiological pulmonary art

146 pping into the phasic activation of arterial baroreceptors, known to be associated with changes in th

147 ings suggest that changes in cardiopulmonary baroreceptor load influence carotid baroreflex resetting

148 luence the changes in heart rate produced by baroreceptor loading or unloading.

149 ak cardiovascular responses to acute carotid baroreceptor loading that may be, in part, due to age-re

150 Cardiopulmonary baroreceptor loading with the supine position appeared t

151 ated by metaboreflex stimulation and not via baroreceptor loading.

152 dulating skin blood flow, but the effects of baroreceptor loading/unloading on sweating are less clea

153 In animal models, distension of baroreceptors located in the pulmonary artery induces a

154 Afferent input from pulmonary arterial baroreceptors may contribute to sympathetic neural activ

155 se seems to be primarily determined by renal baroreceptor mechanisms triggered by reduced blood press

156 orhabditis elegans, may be components of the baroreceptor mechanosensor.

157 that ENaC subunits may be components of the baroreceptor mechanotransducer and pave the way to a bet

158 etic nerve activity (MSNA), likely through a baroreceptor-mediated pathway.

159 ted network mechanisms for the modulation of baroreceptor-mediated reflexes.

160 EG/ENaC members was suggested by blockade of baroreceptor nerve activity and baroreflex control of bl

161 terial pulse (AP) and thus pulse-synchronous baroreceptor nerve activity.

162 Baroreceptor nerve endings detect acute fluctuations in

163 alized to the site of mechanotransduction in baroreceptor nerve terminals innervating the aortic arch

164 litarii, the site of termination of arterial baroreceptor nerves, projects to pontine preganglionic n

165 e assessed GABA transmission in second-order baroreceptor neurones identified by attached aortic depr

166 to suppress GABA release at the second-order baroreceptor neurones.

167 The present study utilized cultured aortic baroreceptor neurons and the styryl dye FM2-10 to charac

168 epolarizing influence of the HCN channels in baroreceptor neurons and their terminals.

169 We found that aortic baroreceptor neurons in the nodose ganglia and their ter

170 ic vesicle exocytosis in primary cultures of baroreceptor neurons is reduced during high-frequency st

171 -cell patch-clamp recordings of second-order baroreceptor neurons revealed that two group II mGluR ag

172 Labelled aortic baroreceptor neurons, immunohistochemistry and an isolat

173 n as autocrine regulators of Na+ currents in baroreceptor neurons.

174 e was identified in fluorescently identified baroreceptor neurons.

175 notropic glutamate receptors on second-order baroreceptor neurons.

176 d evidence that neuronal Kv7 channels in the baroreceptors of the aortic arch adjust the sensitivity

177 from skeletal muscle receptors and arterial baroreceptors onto substance P-containing neurones in th

178 apnoea result from changes of chemoreceptor, baroreceptor or lung stretch receptor inputs.

179 ting no convergence of activity from carotid baroreceptors or aortic baroreceptors with pressure thre

180 neurones responded to activation of carotid baroreceptors or denervation of aortic baroreceptors, in

181 not be attributed to altered chemoreceptor, baroreceptor, or pulmonary stretch receptor activity.

182 ither the magnitude of the responses nor the baroreceptor pressure corresponding to 50 % of the respo

183 Arterial baroreceptors provide a neural sensory input that reflex

184 conclusion, unloading of pulmonary arterial baroreceptors reduced basal sympathetic outflow to the s

185 This study determined baroreceptor reflex (BR) function in conscious rats whic

186 solutions) into the cNTS did not affect the baroreceptor reflex (P > 0.2) while pentobarbitone (100

187 odels describing the coupled function of the baroreceptor reflex and mechanics of the circulatory sys

188 obstructive sleep apnoeic events, alters the baroreceptor reflex and this may lead to hypertension.

189 The baroreceptor reflex bradycardia was depressed significan

190 AT1 receptors in the NTS can depress the baroreceptor reflex bradycardia which is independent of

191 tivity in the NTS for chronically regulating baroreceptor reflex function in conscious rats.

192 iated signaling that includes a reduction in baroreceptor reflex function, presumably via a NADPH-ROS

193 d increase in BP may be due to a decrease in baroreceptor reflex function.

194 1 mM, 50 nl) also significantly reduced the baroreceptor reflex gain (63+/-8%, p<0.05).

195 try in freely moving animals and spontaneous baroreceptor reflex gain (sBRG) determined by a time-ser

196 ood pressure, and an increase in spontaneous baroreceptor reflex gain (sBRG).

197 ve within the NTS and is a factor regulating baroreceptor reflex gain and heart rate.

198 etry data revealed a decrease in spontaneous baroreceptor reflex gain following sEH inhibition, indic

199 ype 1 (AT1) receptor antagonist improves the baroreceptor reflex gain in spontaneously hypertensive r

200 diated depression of cardiac and sympathetic baroreceptor reflex gain in the WKY.

201 Baroreceptor reflex gain measured by the response in hea

202 artially reduced the effect of Ang II on the baroreceptor reflex gain.

203 pear to be involved in the modulation of the baroreceptor reflex in the dlNTS.

204 utamate receptors (mGluRs) in modulating the baroreceptor reflex in the rat NTS.

205 est that a NOS-cGMP signalling system in the baroreceptor reflex pathway distal to the NTS and closer

206 B3/Neuregulin signaling pathway but also the baroreceptor reflex response, which have been functional

207 Cardiac baroreceptor reflex sensitivity (BRS) was impaired in NP

208 elations of heart rate variability (HRV) and baroreceptor reflex sensitivity (BRS) with ambulatory an

209 s of ephedrine on cardiac autonomic control, baroreceptor reflex sensitivity (BRS), heart rate (HR) v

210 Possible mechanisms include improvements in baroreceptor reflex sensitivity and renal function, rest

211 at during exercise the reduction of arterial baroreceptor reflex sensitivity at the operating point w

212 llow-up: pharmacological baroreflex testing (baroreceptor reflex sensitivity), short-term spectral an

213 point analysis, microvolt T wave alternans, baroreceptor reflex sensitivity, and SD of all normal-to

214 resistance and asphyxia cause changes in the baroreceptor reflex which could lead to an increase in b

215 ractus solitarii (NTS) are necessary for the baroreceptor reflex, a primary mechanism for homeostatic

216 pressure to derive phenotypes related to the baroreceptor reflex, a short-term controller of blood pr

217 ular resistance and direct inhibition of the baroreceptor reflex, leading to increased blood pressure

218 urons are involved in the origination of the baroreceptor reflex, they suggest that only a modest par

219 ypertension and possibly with changes in the baroreceptor reflex.

220 charge frequency of the S-A node through the baroreceptor reflex.

221 ch is critically important for mediating the baroreceptor reflex.

222 994, 5 microM) but this had no effect on the baroreceptor reflex.

223 speed would reduce MSNA through the arterial baroreceptor reflex.

224 he baroreflex, all indicative of an impaired baroreceptor reflex.

225 is an important determinant of the arterial baroreceptor reflex.

226 wn that eNOS may contribute to regulation of baroreceptor reflexes and arterial pressure, we examined

227 sing effect of cocaine because activation of baroreceptor reflexes decreases SNA, the neural stimulus

228 ch may subserve respiratory chemosensory and baroreceptor reflexes.

229 nd activation of cardiopulmonary, chemo- and baroreceptor reflexes.

230 between pulmonary arterial and carotid sinus baroreceptor reflexes; physiological and pathological st

231 n the fetal cardiac outflow tract, including baroreceptor regions in the aortic arch, carotid sinus,

232 Vagal sensory innervation to baroreceptor regions of the cardiac outflow tract was co

233 ect different functional roles of neurons in baroreceptor regulation of vasomotor activity.

234 Characterization of baroreceptor-related neurons was performed in 15 anesthe

235 ther emphasizing the connectivity pattern in baroreceptor-related units.

236 rnal influences, including those of arterial baroreceptors, respiration, and other less well-defined

237 ing greater vagal predominance and moderated baroreceptor responses (eg, higher root mean square succ

238 lts, particularly indices of vagal activity, baroreceptor responses, and sinoatrial node function.

239 We performed voltage clamping on NTS baroreceptor second-order neurons in spontaneously hyper

240 onse, compliance), autonomic nervous system (baroreceptor sensitivity and effectiveness), and colonic

241 exercise, and forearm vascular responses and baroreceptor sensitivity were assessed during LBNP using

242 rate turbulence, a noninvasive indicator of baroreceptor sensitivity, has emerged as a simple, pract

243 are independently associated with decreased baroreceptor sensitivity.

244 ity, stress-induced arrhythmia, and impaired baroreceptor sensitivity.

245 nant of autonomic circulatory control and of baroreceptor sensitivity.

246 ynaptic group II mGluRs to further fine-tune baroreceptor signal transmission at the first central sy

247 or postsynaptic group II mGluRs to fine-tune baroreceptor signal transmission in the NTS.

248 ptic role for the Group II mGluRs in shaping baroreceptor signal transmission.

249 both glutamate and GABA release to modulate baroreceptor signal transmission.

250 ibitory inputs that shapes the NTS output of baroreceptor signals.

251 he 3'-untranslated region (3'-UTR) predicted baroreceptor slope (p = 0.014-0.047) and BP change to co

252 Gly/Ser heterozygotes displayed increased baroreceptor slope during upward deflections (by approxi

253 to test the hypothesis that dynamic carotid baroreceptor stimulation (i.e. 5 s trials) using neck pr

254 nly one MnPO-PVN neurone responded solely to baroreceptor stimulation (type IV).

255 Baroreceptor stimulation altered the discharge in subpop

256 ased by baroreceptor unloading, decreased by baroreceptor stimulation and abolished by autonomic gang

257 cent therapeutic approaches based on carotid baroreceptor stimulation and radiofrequency ablation of

258 These results confirm that carotid baroreceptor stimulation causes larger volume changes du

259 In conclusion, acute changes in baroreceptor stimulation did not elicit significant chan

260 Baroreceptor stimulation elicited depressor and bradycar

261 These findings indicate that carotid baroreceptor stimulation elicits dynamic changes in CVC

262 Baroreceptor stimulation was performed by i.v. injection

263 ivity of the vascular resistance response to baroreceptor stimulation was significantly reduced from

264 In conclusion, PE, presumably via baroreceptor stimulation, induces Fos in glutamatergic a

265 ic, circulating angiotensin II (Ang II), and baroreceptor stimulation.

266 econfigured during the respiratory cycle and baroreceptor stimulation.

267 neurones increased their firing rate during baroreceptor stimulation.

268 phe cells decreased their firing rate during baroreceptor stimulation.

269 ttern and frequency of discharge in arterial baroreceptor terminals are, with few exceptions, unknown

270 The data suggest that aortic baroreceptor terminals exhibit frequency-dependent depre

271 that astrocytes may function as intracranial baroreceptors that play an important role in the control

272 not deficits in the responsiveness of aortic baroreceptors to AP.

273 ed afferent activity from pulmonary arterial baroreceptors to investigate their stimulus-response cha

274 lus-response curve of the pulmonary arterial baroreceptors to lower pressures so that it lies within

275 ones transform and transmit information from baroreceptors to neurones in the ventral respiratory gro

276 tion of blood from the heart causes arterial baroreceptors to signal centrally the strength and timin

277 ensory input conveyed from the carotid sinus baroreceptors to the dlNTS is mediated by SP immunoreact

278 The role for substance P (SP) in baroreceptor transmission in the nucleus tractus solitar

279 on pressure and may function as intracranial baroreceptors, tuned to monitor brain blood flow.

280 oreceptor activation (muscle contraction) or baroreceptor unloading (carotid artery occlusion) were s

281 MSNA responses to baroreceptor unloading and the cold pressor test were no

282 sive LBNP (and presumed progressive arterial baroreceptor unloading) increases cross-spectral coheren

283 ities expected of MSNA, and was increased by baroreceptor unloading, decreased by baroreceptor stimul

284 n, which is likely due, at least in part, to baroreceptor unloading.

285 62 years) we changed the stimulus to carotid baroreceptors, using neck chambers and graded pressures

286 at the hypoxic component of asphyxia reduces baroreceptor-vascular resistance reflex sensitivity, whi

287 ed that breathing an asphyxic gas resets the baroreceptor-vascular resistance reflex towards higher p

288 progressive unloading of the cardiopulmonary baroreceptors was attenuated in endurance-trained subjec

289 The stimulus to the carotid baroreceptors was changed using graded pressures of -40

290 sponses to stimulation of pulmonary arterial baroreceptors were altered by intrathoracic pressure cha

291 rtic arch, carotid sinus and coronary artery baroreceptors were controlled.

292 Pressures distending carotid and aortic baroreceptors were controlled.

293 Baroreceptors were stimulated by applying pressure incre

294 Baroreceptors were stimulated by raising perfusion press

295 ted sinus or selective denervation of aortic baroreceptors were used to test for convergent excitatio

296 reflex mediated by aortic and carotid sinus baroreceptors when systemic arterial pressure is lowered

297 eads to increased distortion of the arterial baroreceptors with a subsequent decline in MSNA.

298 ctivity from carotid baroreceptors or aortic baroreceptors with pressure thresholds of approximately

299 In contrast, conditioning carotid baroreceptors with the same regime produced significant

300 which is primarily mediated by the arterial baroreceptors, with a modest cardiopulmonary vasodepress