ライフサイエンスコーパス: baroreflex

1 apnea incidence, and desensitization of the baroreflex.

2 hanism may be sympathetic activation via the baroreflex.

3 s and enhanced the gain of the fetal cardiac baroreflex.

4 Thus, its upregulation does not augment the baroreflex.

5 nd used to assess changes in the muscle-pump baroreflex.

6 iating dorsal PAG modulation of the arterial baroreflex.

7 minate dorsal PAG attenuation of the cardiac baroreflex.

8 echanical and neural aspects of the arterial baroreflex.

9 Following baroreflex ablation with trimethaphan (3-7 mg min(1)), c

10 s have exposed potential differences between baroreflex activation and RDN and common challenges that

11 hat account for blood pressure lowering with baroreflex activation and RDN and, in so doing, have pro

12 c insights into blood pressure lowering with baroreflex activation and RDN in the context of progress

13 2) the systolic blood pressure threshold for baroreflex activation increases significantly (the baror

14 Carotid baroreflex activation lowers blood pressure and might ha

15 demonstrated the safety and effectiveness of baroreflex activation therapy (BAT) in patients with hea

16 We sought to determine the effect of baroreflex activation therapy (BAT) on systolic blood pr

17 (Baroreflex Activation Therapy for Heart Failure [BeAT-HF

18 The BeAT-HF (Baroreflex Activation Therapy for Heart Failure) trial w

19 roaches, transcatheter renal denervation and baroreflex activation therapy, are used in clinical prac

20 Unilateral electrical baroreflex activation, endovascular baroreflex amplifica

21 hypothesized that selective manipulation of baroreflex activity through electrical carotid sinus sti

22 expression of nNOS in the NTS of rats whose baroreflex activity was then studied.

23 a novel regulatory function of FGF21 in the baroreflex afferent pathway (the nucleus tractus solitar

24 ontrol of blood pressure regulations through baroreflex afferent pathway in HFD rats.

25 the circulation, and a decreased gain of the baroreflex, all indicative of an impaired baroreceptor r

26 al chemoreflex, diving response and arterial baroreflex, allowing the discrimination of muscle vasoco

27 The muscle-pump baroreflex also had decreased gain and fraction time act

28 ectrical baroreflex activation, endovascular baroreflex amplification and pacemaker-mediated cardiac

29 y with electrical stimulation of the carotid baroreflex and catheter-based renal denervation (RDN).

30 served increase in the reflex sensitivity of baroreflex and chemoreflex in in situ preparation.

31 t working heart-brainstem preparation during baroreflex and chemoreflex stimulation or with carbachol

32 fetal body and breathing movements, and from baroreflex and circadian processes.

33 NOS, resulting in activation of the arterial baroreflex and subsequent inhibition of central sympathe

34 ho-inhibitory and bradycardiac components of baroreflex and the sympathetic and respiratory responses

35 defibrillators; neurohumoral modification by baroreflex and vagal stimulation; prevention of adverse

36 , the first synaptic station of afferents of baroreflexes and chemoreflexes, were evaluated using bra

37 solitarii (NTS) of rat, attenuates arterial baroreflexes, and leads to lability of arterial blood pr

38 ese data suggest that attenuated sympathetic baroreflexes are the result of altered central mechanism

39 t the rostral-ventrolateral medulla, altered baroreflex blood pressure regulation and death from stro

40 size within each burst is augmented for the baroreflex BP control despite the impaired response of b

41 capnia also causes resetting of the arterial baroreflex, but that this resetting would not occur with

42 minance, and (iii) resetting of the arterial baroreflex causes immediate exercise-onset reflexive inc

43 During each condition, carotid baroreflex (CBR) function was determined using the rapid

44 ed optical mapping to measure the effects of baroreflex, chemoreflex and carbachol on pacemaker entra

45 s immunoreactivity (Fos-IR) in the hindbrain baroreflex circuit.

46 , we hypothesized that mechanical and neural baroreflex components contribute equally to baroreflex h

47 ctivity, and (3) if mechanical and/or neural baroreflex components related to differences in integrat

48 hich was accompanied by improvements in both baroreflex control and spectral indicators of cardiac sy

49 Furthermore, arterial baroreflex control at HA may be influenced by genotypic

50 e B (TrkB) receptor signalling in the NTS on baroreflex control both in healthy and CHF rats.

51 arterial pressure and MSNA, but sympathetic baroreflex control is reduced before presyncope; (2) wit

52 Thus, other factors rather than sympathetic baroreflex control mechanisms contribute to sex differen

53 itarius (NTS) is essential for orchestrating baroreflex control of blood pressure.

54 Administration of E2 increased baroreflex control of heart rate (derived from the modif

55 essure (MAP) but did significantly attenuate baroreflex control of heart rate (HR) evoked by low freq

56 The baroreflex control of heart rate (HR) is reduced followi

57 Baroreflex control of heart rate (n = 16) and muscle sym

58 ptors with isocapnic hypoxia resets arterial baroreflex control of heart rate and sympathetic vasocon

59 -3 mm Hg) and HR (33+/-3 bpm) and attenuated baroreflex control of HR at both ADN stimulation frequen

60 he nucleus ambiguus (NA) plays a key role in baroreflex control of HR, we examined whether CIH remode

61 None of the treatments altered MAP, HR, or baroreflex control of HR.

62 al LSNA (to 228 +/- 28% control) and gain of baroreflex control of LSNA (from 3.8 +/- 1.1 to 7.4 +/-

63 insulin increased LSNA and HR and baroreflex control of LSNA and HR in non-pregnant rats,

64 i.c.v. insulin infusion increased basal and baroreflex control of LSNA and HR similarly in pro-oestr

65 eases lumbar (LSNA) and renal (RSNA) SNA and baroreflex control of LSNA and RSNA in alpha-chloralose

66 otherwise untreated rats increased basal and baroreflex control of LSNA, indicating that endogenous N

67 ies indicate that insulin increases arterial baroreflex control of lumbar sympathetic nerve activity;

68 e vasculature and reset vascular-sympathetic baroreflex control of MSNA downward and leftward in heal

69 We show that the arterial baroreflex control of MSNA functions normally in healthy

70 Acute hyperoxia at HA had minimal effect on baroreflex control of MSNA in Lowlanders and Sherpa, rai

71 vity (MSNA); however, the effect on arterial baroreflex control of MSNA is unknown.

72 t rest, whole-body heating enhanced arterial baroreflex control of MSNA through increased sensitivity

73 The sensitivity of baroreflex control of MSNA was unchanged during DEH comp

74 mine the gain (i.e. sensitivity) of arterial baroreflex control of MSNA.

75 plasma insulin enhance the gain of arterial baroreflex control of MSNA.

76 (modified Oxford test) were used to evaluate baroreflex control of MSNA.

77 been used to describe two sites for arterial baroreflex control of MSNA.

78 pressure influenced sympathetic outflow and baroreflex control of muscle sympathetic nerve activity

79 lex mechanism, we tested the hypothesis that baroreflex control of muscle sympathetic nerve activity

80 creased sympathetic nerve activity (SNA) and baroreflex control of SNA and heart rate more dramatical

81 lumbar, splanchnic and renal SNA, as well as baroreflex control of SNA.

82 contrast, i.c.v. leptin increased basal and baroreflex control of splanchnic SNA (SSNA) and heart ra

83 rat medial nTS (mnTS), a region critical for baroreflex control of sympathetic outflow, produced dose

84 Baroreflex control of the heart rate is significantly re

85 <0.05) and increased the maximal gain of the baroreflex curves for heart rate (2.2+/-0.2 to 4.6+/-0.7

86 logical control system, such as the arterial baroreflex, depends critically upon both the magnitude (

87 g the central alterations that contribute to baroreflex desensitization during CHF.

88 The baroreflex desensitization in CHF is at least partly the

89 that contributes to sympatho-excitation and baroreflex desensitization.

90 ole in arterial pressure maintenance via the baroreflex during acute orthostasis in humans.

91 greater neural component of the sympathetic baroreflex during both pressure falls and pressure rises

92 bles were related to the presence/absence of baroreflex dysfunction (defined by spontaneous barorefle

93 were more frequent in surgical patients with baroreflex dysfunction (relative risk, 1.66 [95% CI, 1.1

94 acic echocardiography following experimental baroreflex dysfunction (sino-aortic denervation) in rats

95 We hypothesized that baroreflex dysfunction alone is sufficient to cause card

96 eceptor kinase 2 expression in conditions of baroreflex dysfunction and preserved cardiac function.

97 Baroreflex dysfunction in patients was also associated w

98 Experimental baroreflex dysfunction in rats and mice resulted in impa

99 Baroreflex dysfunction was present in 81 of 249 patients

100 The associations of baroreflex dysfunction with intraoperative cardiac funct

101 betes, those with type 2 diabetes show early baroreflex dysfunction, likely due to insulin resistance

102 Afferent baroreflex failure is most often due to damage of the ca

103 ta show a significantly impaired muscle-pump baroreflex following bedrest.

104 re evaluated for heritable autonomic traits: baroreflex function and pressor response to environmenta

105 gnalling in the dmNTS is integral for normal baroreflex function as indicated by the blunting of baro

106 smitters and neuromodulators in the dmNTS on baroreflex function both in normal and CHF states is not

107 were differences in sympathetic activity and baroreflex function by age, sex, or physical activity st

108 ermine if resetting of the carotid-vasomotor baroreflex function curve during exercise is modulated b

109 comparison to control, the carotid-vasomotor baroreflex function curve was relocated downward and lef

110 gal control of the heart rate and attenuated baroreflex function during aging.

111 lved in descending modulation of the cardiac baroreflex function during defensive behavior.

112 entional wisdom, hysteresis in cardiac vagal baroreflex function exhibits a specific pattern: pressur

113 0% oxygen did not alter vascular sympathetic baroreflex function for either group at HA.

114 stem, without changing intrinsic sympathetic baroreflex function in elderly hypertensive patients.

115 of arterial pressure and impairment of vagal baroreflex function in space.

116 Impairment of baroreflex function is associated with the progression o

117 of vasomotor responsiveness and sympathetic baroreflex function is not the cause of neurally mediate

118 ysical activity status, (2) if any aspect of baroreflex function related to differences in resting sy

119 flex activation increases significantly (the baroreflex function shifts to the right; 120 +/- 14 vs.

120 Cardiac vagal baroreflex function was assessed using the modified Oxfo

121 Baroreflex function was further assessed during a Valsal

122 Blood pressure and baroreflex function was reduced in double knockout mice,

123 Baroreflex function was similar between groups.

124 amic arterial elastance and arterial-cardiac baroreflex function were calculated by transfer function

125 Indices of vascular sympathetic baroreflex function were determined from the relationshi

126 cal role of glycinergic neurotransmission in baroreflex function, identify the mechanisms for glycine

127 hypertension and restored ACE2 activity and baroreflex function.

128 vasopressor response to Ang II and impaired baroreflex function.

129 to measure sympathetic, parasympathetic, and baroreflex function.

130 oreceptors does not appear to alter arterial baroreflex function.

131 PAG-evoked increases in MAP, HR and cardiac baroreflex function.

132 crease in sympathetic drive and resetting of baroreflex function.

133 amic arterial elastance and arterial-cardiac baroreflex function.

134 amic arterial elastance and arterial-cardiac baroreflex function.

135 /- 19, 6 nU; and 205 +/- 28, 60 nU) and LSNA baroreflex gain (in % control mmHg-1 from 4.3 +/- 1.2 to

136 raction: P = 0.008) and the arterial-cardiac baroreflex gain (P = 0.005) were significantly increased

137 heart rate (P = 0.6) or vascular-sympathetic baroreflex gain (P = 0.85).

138 explore the explanatory power of integrated baroreflex gain and its mechanical and neural components

139 Baroreflex gain and its mechanical and neural components

140 the antagonization of TrkB, which inhibited baroreflex gain and range.

141 etrics changed in opposite directions: vagal baroreflex gain and two indices of vagal fluctuations (r

142 etrics changed in opposite directions: vagal baroreflex gain and two indices of vagal fluctuations ro

143 e the sympathetic nervous system and enhance baroreflex gain are well known, the specific brain site(

144 of P2Y(1) purinoceptors in the NTS decreased baroreflex gain by 40% (p = 0.031), whereas blockade of

145 ereas blockade of P2Y(1) receptors increased baroreflex gain by 57% (p = 0.018).

146 rvals declined by 14% (P = 0.003), and vagal baroreflex gain by 9% (P = 0.009).

147 ATP in the NTS would be expected to decrease baroreflex gain by the mechanism described here.

148 resting sympathetic outflow nor sympathetic baroreflex gain components.

149 ; altered arterial baroreceptor input (vagal baroreflex gain declined and muscle sympathetic nerve bu

150 Sympathetic baroreflex gain may be reduced, and muscle sympathetic f

151 ivity (LSNA) were recorded continuously, and baroreflex gain of HR and LSNA were measured before and

152 Baroreflex gain was not altered by hyperpnoea or hyperca

153 Starling mechanism gain and arterial-cardiac baroreflex gain were significantly increased in the exer

154 es ( approximately 0.25 Hz) lowered arterial baroreflex gain, and provoked smaller arterial pressure

155 the sympathetic nervous system and increase baroreflex gain, via a neural pathway that includes the

156 hown to either increase, or not change vagal baroreflex gain.

157 ponents related to differences in integrated baroreflex gain.

158 t in conjunction to determine differences in baroreflex gain.

159 ure, sympathetic vasoconstrictor outflow, or baroreflex gain.

160 flow to higher pressures, without changes in baroreflex gain.

161 Baroreflex heart rate responses to phenylephrine-induced

162 ull expression of PEH requires a functioning baroreflex, hypertension, and activation of muscle affer

163 ls, and therefore it has been suggested that baroreflex hysteresis derives solely from vascular behav

164 baroreflex components contribute equally to baroreflex hysteresis.

165 responses to phenylephrine were enhanced and baroreflexes impaired in these animals.

166 parately as subcomponents of the sympathetic baroreflex in older adults, and we found that the distri

167 red neurons and Ang II-induced inhibition of baroreflex in spontaneously hypertensive rats (SHR) vers

168 tudy examined whether attenuated sympathetic baroreflexes in OZRs may be due to altered sensory or ce

169 this confounding inhibitory influence of the baroreflex, in the current study we directly measured sk

170 The arterial baroreflex is a rapid negative-feedback system that comp

171 We found that the non-cardiac SNA baroreflex is active over a lower range of pressures tha

172 echanism of how the central component of the baroreflex is affected in pathological conditions.

173 For example the baroreflex is altered during a stress response or exerci

174 Impaired baroreflex may contribute to the development of cardiova

175 Arterial baroreflexes may regulate resistance vessels supplying g

176 blood pressure (BP) is regulated through the baroreflex mechanism, we tested the hypothesis that baro

177 ear signals, potentially implicating central baroreflex mechanisms for anxiolytic treatment targets.

178 hesis that spaceflight does not impair human baroreflex mechanisms.

179 ual breathing frequencies are unlikely to be baroreflex mediated, and disappear during apnoea.

180 ctuations at usual breathing frequencies are baroreflex mediated, that they persist during apnoea, an

181 However, cardiovagal baroreflex-mediated bradycardia during a hypertensive st

182 l influences with atropine similarly reduced baroreflex-mediated bradycardic responses to increases i

183 Baroreflex-mediated changes in sympathetic vasomotor ton

184 Furthermore, E2 administration increases baroreflex-mediated heart rate responses to orthostasis

185 nL) into the RVLM decreased the duration of baroreflex-mediated inhibition of renal sympathetic nerv

186 ower body negative pressure (LBNP; activates baroreflex-mediated sympathetic system) and the cold pre

187 The baroreflex MSNA operating point and resting sympathetic

188 Similarly, after meal intake, arterial baroreflex-MSNA gain for burst incidence and total MSNA

189 fasting insulin concentrations, the arterial baroreflex-MSNA gain remained unchanged.

190 le glucose was maintained constant, arterial baroreflex-MSNA gain was similarly enhanced (e.g. burst

191 During baroreflex onset, the capacity of the central region to

192 lar resistance (SVR), possibly confounded by baroreflexes or interactions between single nucleotide p

193 insic inhibitory input to the neurons in the baroreflex pathway.

194 hesis that nNOS is involved in excitation of baroreflex pathways in NTS while excluding pharmacologic

195 nNOS in the NTS is integral to excitation of baroreflex pathways involved in reflex tachycardia, a la

196 e too short and variable to be attributed to baroreflex physiology.

197 attenuated in habitual smokers; that is, the baroreflex plays a permissive role, allowing sympathoexc

198 to elicit sigmoid, vagally mediated carotid baroreflex R-R interval responses.

199 creasing CBV and loading the cardiopulmonary baroreflex reduces the magnitude of exercise-induced inc

200 ndently suppressed lumbar SNA (LSNA) and its baroreflex regulation, and these effects were blocked by

201 ctivation contribute to vascular sympathetic baroreflex resetting and sympathoexcitation.

202 ulmonary baroreceptor load influence carotid baroreflex resetting during dynamic exercise.

203 in healthy Lowlanders at HA, and that upward baroreflex resetting permits chronic activation of basal

204 For Lowlanders, upward baroreflex resetting promotes heightened sympathetic vas

205 d chronotropic responses manifested the same baroreflex responses as animals that had been treated wi

206 Neither AAV2 eGFP nor AAV2nNOScDNA affected baroreflex responses.

207 e influence of ageing on the latency of peak baroreflex responses.

208 -2 (0.4 mmol/l) into the mNTS attenuated the baroreflex responses.

209 st) into the mNTS (0.5 mmol/l) did not alter baroreflex responses.

210 ticularly important and occurs via augmented baroreflex responsiveness and increased cardiomyocyte se

211 ents (muscle metaboreflex) decreases cardiac baroreflex responsiveness during leg cycling exercise in

212 fferences in the cardiovagal and sympathetic baroreflex sensitivities between phases under any condit

213 antecedent hypoglycemia leads to 1) reduced baroreflex sensitivity (16.7 +/- 1.8 vs. 13.8 +/- 1.4 ms

214 Baroreflex sensitivity (adjusted odds ratio, 0.9; p = 0.

215 systolic blood pressure, cardiac parameters, baroreflex sensitivity (BRS) and hyperinsulinemia in the

216 This study sought to evaluate cardiac baroreflex sensitivity (BRS) as a predictor of response

217 lex function as indicated by the blunting of baroreflex sensitivity (BRS) following the antagonizatio

218 Sympathetic baroreflex sensitivity (BRS) is greater during decreasin

219 Impaired baroreflex sensitivity (BRS) predicts cardiovascular mor

220 Sympathetic baroreflex sensitivity (BRS) was assessed.

221 Also, we analysed sympathetic baroreflex sensitivity (BRS) with burst occurrence and a

222 ventilatory recruitment threshold (VRT-CO2), baroreflex sensitivity (BRS), blood pressure, and blood

223 ailure (CHF) results in blunting of arterial baroreflex sensitivity (BRS), which arises from alterati

224 es in sympathetic activity and reductions in baroreflex sensitivity (BRS).

225 mental stress, as well as impaired arterial baroreflex sensitivity (BRS).

226 nism for the decrease in spontaneous cardiac baroreflex sensitivity (cBRS) during exercise in humans.

227 thetic nerve activity (MSNA) and sympathetic baroreflex sensitivity (MSNA-diastolic pressure relation

228 emetry), autonomic function, and spontaneous baroreflex sensitivity (SBRS) were not significantly dif

229 Fortunately, emerging data suggest that baroreflex sensitivity and autonomic function may be res

230 Baroreflex sensitivity and the sympathetic response to h

231 Cardiovagal baroreflex sensitivity assessed during decreasing BP (i.

232 Sympathetic baroreflex sensitivity assessed with burst incidence was

233 The spontaneous baroreflex sensitivity at baseline was significantly low

234 Similar sympathetic baroreflex sensitivity between sexes and phases was also

235 t-negative SNARE protein (dnSNARE) increased baroreflex sensitivity by 70% (p < 0.001).

236 ared with baseline euglycemic conditions, 1) baroreflex sensitivity decreases significantly (19.2 +/-

237 Sympathetic baroreflex sensitivity did not differ between sexes (P =

238 d HR increase, systolic function impairment, baroreflex sensitivity drop, as well as pulse interval v

239 MSNA, haemodynamic responses and baroreflex sensitivity during early tilting were not dif

240 athetic neural responses but not sympathetic baroreflex sensitivity during orthostasis, though uprigh

241 rterial pressure, sympathovagal balance, and baroreflex sensitivity for control of heart rate.

242 mpathetic nerve activity and reduced cardiac baroreflex sensitivity heighten cardiovascular risk, alt

243 nin activity, aldosterone, urine sodium, and baroreflex sensitivity in both groups.

244 hough studies have examined resting arterial baroreflex sensitivity in older subjects, little attenti

245 mpathetic nerve activity and reduced cardiac baroreflex sensitivity in patients with RA compared to m

246 of ANA-12 into the dmNTS greatly diminished baroreflex sensitivity in sham rats, whereas it had less

247 e, and normalized heart rate variability and baroreflex sensitivity in TGA-PE rats compared to contro

248 s measurements of heart rate variability and baroreflex sensitivity in the neuromonitoring setting of

249 Reduced baroreflex sensitivity is associated with nicotinamide a

250 Not only sympathetic but also cardiovagal baroreflex sensitivity is similar between sexes and mens

251 roreflex dysfunction (defined by spontaneous baroreflex sensitivity of <6 ms mm Hg).

252 Baroreflex sensitivity showed no correlation with intrac

253 endent astroglial release of ATP to modulate baroreflex sensitivity via P2Y(1) receptors.

254 at process afferent information and modulate baroreflex sensitivity via the release of ATP.

255 Baroreflex sensitivity was assessed every 10 seconds usi

256 Baroreflex sensitivity was assessed in the time domain w

257 Sympathetic baroreflex sensitivity was quantified using the slope of

258 Sympathetic baroreflex sensitivity was quantified using the slope of

259 s measurements of heart rate variability and baroreflex sensitivity we aimed to test whether autonomi

260 s of RR interval variability and spontaneous baroreflex sensitivity were also computed.

261 Sympathovagal balance and spontaneous baroreflex sensitivity were restored during vitamin C in

262 Similar changes in baroreflex sensitivity were seen.

263 art rate variability, heart rate turbulence, baroreflex sensitivity) were significant predictors of a

264 We have previously shown that depressed baroreflex sensitivity, an established marker of reduced

265 ngiotensin II levels, inflammation, impaired baroreflex sensitivity, and autonomic dysfunction, as we

266 stress, impaired sympathetic and cardiovagal baroreflex sensitivity, and increased inflammation.

267 ormalized indexes of sympathetic outflow and baroreflex sensitivity, and reduced the incidence of apn

268 aimed to evaluate left ventricular function, baroreflex sensitivity, autonomic modulation, and inflam

269 ween arrhythmic events and predictive tests (baroreflex sensitivity, heart rate turbulence, heart rat

270 Mean values of baroreflex sensitivity, heart rate variability, intracra

271 upled with impairments in renal function and baroreflex sensitivity, increased neuroinflammatory mark

272 eart rate variability, endothelial function, baroreflex sensitivity, inflammation, and platelet funct

273 t, as measured by heart rate variability and baroreflex sensitivity, is significantly associated with

274 function, including decreased cardiac vagal baroreflex sensitivity, may contribute directly to morta

275 fects heart rate, blood pressure regulation, baroreflex sensitivity, tissue oxygenation, and vascular

276 stiffness; (2) it is associated with reduced baroreflex sensitivity, which increases blood pressure v

277 amic Starling mechanism and arterial-cardiac baroreflex sensitivity, without changing dynamic arteria

278 heart, leading to hypertension and depressed baroreflex sensitivity.

279 vs. sham-operated SHR) and an improvement in baroreflex sensitivity.

280 trual cycle had no influences on cardiovagal baroreflex sensitivity.

281 ssed according to heart rate variability and baroreflex sensitivity.

282 renal sympathetic nerve activity and to test baroreflex sensitivity.

283 amic Starling mechanism and arterial-cardiac baroreflex sensitivity.

284 ivity and negatively correlated with cardiac baroreflex sensitivity.

285 an increase in parasympathetic activity and baroreflex sensitivity.

286 tatory or inhibitory role in transmission of baroreflex signals in the nucleus tractus solitarii (NTS

287 w and previously published studies involving baroreflex stimulation and pharmacological blockade of t

288 nervation, cervical vagal nerve stimulation, baroreflex stimulation, cutaneous stimulation, novel dru

289 esia, low-level vagal nerve stimulation, and baroreflex stimulation.

290 t-term exposure to RHA shifts ('resets') the baroreflex stimulus-response curve to higher levels of B

291 Furthermore, we propose that baroreflex suppression of sympathetic activation is atte

292 lays a critical role in maintaining arterial baroreflex sympathoinhibition.

293 point'), as well as during a modified Oxford baroreflex test (i.e. 'gain').

294 ears, and a final follow-up: pharmacological baroreflex testing (baroreceptor reflex sensitivity), sh

295 OS in turn activate chemoreflex and suppress baroreflex, thereby stimulating the sympathetic nervous

296 y and BRS was measured using the spontaneous baroreflex threshold technique.

297 a lower range of pressures than the cardiac baroreflex (threshold 66 +/- 1 mmHg versus 82 +/- 5 mmHg

298 Baroreflex trials were separated by 30 min of rest.

299 Causality of the muscle-pump baroreflex was reduced on R0 (0.73 +/- 0.2) compared to

300 Both handgrip (HG) and disengagement of baroreflexes with lower body negative pressure (LBNP) ca