ライフサイエンスコーパス: vasodilatation

1 onstriction while decreases in PO2 result in vasodilatation.

2 hyperpolarization and endothelium-dependent vasodilatation.

3 saline did not affect sweating or cutaneous vasodilatation.

4 ression of exogenous H2 S-mediated cutaneous vasodilatation.

5 05), whereas SNP did not impact ACh-mediated vasodilatation.

6 mune disorders, in the modulation of carotid vasodilatation.

7 Na2 S and NaHS elicited dose-dependent vasodilatation.

8 nitroprusside was perfused to elicit maximal vasodilatation.

9 on vascular permeability, angiogenesis, and vasodilatation.

10 omas, processes, and end-feet preceded local vasodilatation.

11 ra-arterial blood pressure to quantify local vasodilatation.

12 cellular pathway that coordinates spreading vasodilatation.

13 ced vasoconstriction and hypercapnia-induced vasodilatation.

14 l-NAME was perfused to quantify NO-dependent vasodilatation.

15 mutually required to elicit angiogenesis and vasodilatation.

16 unction resulting in impaired EDHF-dependent vasodilatation.

17 ation, a reduction in global [Ca(2)(+)]i and vasodilatation.

18 romote K(V)1 channel expression and cerebral vasodilatation.

19 trapezius blood flow/ABP), indicating muscle vasodilatation.

20 lateau in all sites to quantify NO-dependent vasodilatation.

21 nces on vascular tone and thus isolate local vasodilatation.

22 heating (42 degrees C) induced NO-dependent vasodilatation.

23 othelial purinergic receptors and stimulates vasodilatation.

24 hysical activity enhances insulin-stimulated vasodilatation.

25 ercise-induced amplification of ACh-mediated vasodilatation.

26 hysical activity enhances insulin-stimulated vasodilatation.

27 st BIBP3226, BIBN4096bs partly inhibited the vasodilatation.

28 hysical activity enhances insulin-stimulated vasodilatation.

29 uced a profound hypothermia due to cutaneous vasodilatation.

30 such as angiogenesis, glucose tolerance, and vasodilatation.

31 P = 0.001 vs. controls) caused by cutaneous vasodilatation.

32 ults without parallel increases in cutaneous vasodilatation.

33 ood flow responses and endothelium-dependent vasodilatation.

34 exposure, despite peripheral limitations to vasodilatation.

35 ing no effect on beta2-mediated hindquarters vasodilatation.

36 apoAI) and flicker-light retinal arteriolar vasodilatation (0.33%; P = 0.003) and was associated inv

37 /- 0.18 degrees C, P </= 0.01) and cutaneous vasodilatation (+1.15 +/- 0.18 vs. +1.53 +/- 0.22 degree

38 ing rhythmic twitch contractions, slow onset vasodilatation (10-15 s) in FAs remained intact followin

39 via electrical field stimulation produced a vasodilatation (19.4 +/- 1.2 mum, n = 12) that was signi

40 reduced by phosphate loading (median maximum vasodilatation 3.38% [IQR 2.57-5.26] vs 8.4 [6.2-11.6],

41 blood cell flux during local heating-induced vasodilatation (42 degrees C).

42 d with normal phosphate in rat (mean maximum vasodilatation 64% [SE 9] vs 95 [1], p<0.001) and human

43 +/- 4% CVC(max), P < 0.001) and NO-dependent vasodilatation (68 +/- 3% CVC(max), P < 0.001).

44 ficantly correlated with augmented sustained vasodilatation after sympathetic stimulation.

45 as less effective at increasing NO-dependent vasodilatation after the drug intervention (BH(4): 60 +/

46 bition of NO and COX attenuated H2 S-induced vasodilatation (all P < 0.05).

47 and older males, it does modulate cutaneous vasodilatation, although the magnitude of increase is si

48 ating that KNDy neurons facilitate cutaneous vasodilatation, an important heat dissipation effector.

49 tment during increased nitric oxide-mediated vasodilatation and angiopoietin signalling (NO-Tie-media

50 ercise and hypoxia produces a 'compensatory' vasodilatation and augmented blood flow in contracting s

51 ults can achieve greater levels of cutaneous vasodilatation and cardiac output during passive heating

52 passive heat stress, augments both cutaneous vasodilatation and cardiac output in healthy older human

53 s maximally restrain the levels of cutaneous vasodilatation and cardiac output that healthy older adu

54 ctions are characterized by pulmonary venous vasodilatation and fluid extravasation, which are though

55 tation may explain impairments in both local vasodilatation and functional sympatholysis with advanci

56 hysical activity improves insulin-stimulated vasodilatation and glucose uptake.

57 ders the complex signals capable of inducing vasodilatation and hyporesponsiveness to vasoconstrictor

58 haust inhalation was associated with reduced vasodilatation and increased ex vivo thrombus formation

59 ed with local anaesthesia results in greater vasodilatation and increases short-term blood flow.

60 on in patients with more advanced degrees of vasodilatation and inflammation; these changes in LV fun

61 P-activated protein kinase (AMPK) results in vasodilatation and is therefore a potential therapeutic

62 may reduce BP through enhanced eNOS-mediated vasodilatation and may be a novel therapeutic approach f

63 es into the circulation, where it stimulates vasodilatation and natriuresis.

64 evidence that KNDy neurons promote cutaneous vasodilatation and participate in the E(2) modulation of

65 ration of C5a (anaphylatoxin), a promoter of vasodilatation and permeability.

66 hether this system contributes to splanchnic vasodilatation and portal hypertension in cirrhosis.

67 ce of an unaltered shear stress stimulus for vasodilatation and reduced resting steady-state nitric o

68 Nitrite would thus provide local vasodilatation and restore a balance between oxygen supp

69 rofuse physiological elevations in cutaneous vasodilatation and sweating that are accompanied by redu

70 hether ET-1 attenuates cholinergic cutaneous vasodilatation and sweating through a nitric oxide synth

71 s that ET-1 attenuates cholinergic cutaneous vasodilatation and sweating through a nitric oxide synth

72 ived product) may directly mediate cutaneous vasodilatation and sweating through nitric oxide synthas

73 ntense heat, profuse elevations in cutaneous vasodilatation and sweating, and reduced brain blood flo

74 utes to the heat loss responses of cutaneous vasodilatation and sweating, and this may be mediated by

75 se ageing attenuates COX-dependent cutaneous vasodilatation and sweating.

76 ) contributes to the regulation of cutaneous vasodilatation and sweating; however, the mechanism(s) u

77 Primary ageing markedly attenuates cutaneous vasodilatation and the increase in cardiac output during

78 diac functions limit the extent of cutaneous vasodilatation and the increase in cardiac output that h

79 passive-limb movement to assess NO-mediated vasodilatation and therefore NO bioavailability.

80 thetic activation in young men is pronounced vasodilatation and this effect is lost with age as the r

81 ish the role of Kir channels in flow-induced vasodilatation and to provide first insights into the me

82 substrates besides angiotensin II to control vasodilatation and vascular permeability.

83 II repeat of fibrillar FN (FNIII1H) mediates vasodilatation, and (ii) this response is EC dependent.

84 cent vessels with increases in permeability, vasodilatation, and edema are hallmarks of inflammatory

85 oconstriction, reduced endothelium-dependent vasodilatation, and enhanced hypoxic pulmonary vasoconst

86 th remarkably elevated plasma levels of C5a, vasodilatation, and increased vascular permeability.

87 ares of inflammation, itching, burning pain, vasodilatation, and redness of the extremities consisten

88 iontophoresis, flicker-light-induced retinal vasodilatation, and retinal vascular tortuosity.

89 ns (PGs) contribute independently to hypoxic vasodilatation, and that combined inhibition would revea

90 Exposure to acute systemic hypoxia caused vasodilatation, and the response was similar in beta93C

91 Na(+) /K(+) -ATPase, attenuated ATP-mediated vasodilatation ( approximately 35 and approximately 60%

92 Most studies on perivascular nerve-mediated vasodilatation are made in vitro.

93 tin treatment-induced improvements in reflex vasodilatation are mediated, in part, by increases in en

94 Mechanisms by which H(2)S induces vasodilatation are unclear.

95 d not be explained by a reduced stimulus for vasodilatation as group and condition effects persisted

96 KEY POINTS: In response to exercise, vasodilatation ascends from downstream arterioles into u

97 .9, 9.2; P = 0.03) and NO-mediated cutaneous vasodilatation at 42 degrees C heating by 19.6% CVCmax (

98 ic exercise hyperaemia and abolishes hypoxic vasodilatation at rest.

99 Vasodilatation at the plateau and NO-dependent vasodilat

100 Ascending vasodilatation (AVD) is essential for reducing FA resist

101 max); combo 95 +/- 3% CVC(max); NO-dependent vasodilatation BH(4): 68 +/- 3% CVC(max); combo 58 +/- 4

102 Sweat rate, cutaneous vasodilatation, blood pressure, heart rate and middle ce

103 ng the extracellular [K(+) ] to 20 mm caused vasodilatation but was converted to vasoconstriction in

104 thelin B receptor (ET(B) R) subtype mediates vasodilatation, but is blunted in women with PCOS.

105 onstrated a decline in endothelium-dependent vasodilatation, but restored the functional response und

106 indicate that repeated RIPC augments maximal vasodilatation, but the underlying mechanism for this im

107 aining also mediated reductions in cutaneous vasodilatation by 9% (6-12%) at the chest and by 7% (4-9

108 Higher endothelium-dependent vasodilatation by ACh or leptin was abolished with incub

109 tor channel inhibitor, reduced H(2)S-induced vasodilatation by approximately 38 and approximately 37%

110 e onset threshold for sweating and cutaneous vasodilatation by inhibiting efferent thermoregulatory a

111 zation induced by nitric oxide (NO)-mediated vasodilatation, by comparing the phenotype of new microv

112 We conclude that stimulation of EDH-like vasodilatation can blunt alpha1 -adrenergic vasoconstric

113 egulation of vascular tone consists of major vasodilatation caused by CGRP (and possibly substance P)

114 sodilatation, which contrasts with a smaller vasodilatation caused by endogenous CGRP that is only vi

115 bsequently exhibited greater insulin-induced vasodilatation compared to arterioles kept under no-flow

116 , leukocyte count, and endothelium-dependent vasodilatation conferred an increased risk of mortality.

117 Impaired CPT-induced coronary vasodilatation could not be explained by a reduced stimu

118 pressed as a percentage of maximal cutaneous vasodilatation (CVCmax)] were analysed using general lin

119 reduced with age, and endothelium-dependent vasodilatation declines with age in coronary resistance

120 Exercise augmented peak ACh-mediated vasodilatation (DeltaFVC saline: 117 +/- 14; exercise: 2

121 to ACh, exercise did not alter SNP-mediated vasodilatation (DeltaFVC saline: 158 +/- 35; exercise: 1

122 infusion of KCl amplified peak ACh-mediated vasodilatation (DeltaFVC saline: 97 +/- 15, KCl: 142 +/-

123 Current therapies for PH, focusing on vasodilatation, do not normalize these activated phenoty

124 We also show that K(IR) channels augment vasodilatation during exercise which demands greater mus

125 ction contribute to blunted reflex cutaneous vasodilatation during heat stress in healthy older adult

126 the onset for sweat production and cutaneous vasodilatation during heat stress in humans; however, th

127 y delays the onset of sweating and cutaneous vasodilatation during heat stress.

128 ant) improves NO-dependent forearm cutaneous vasodilatation during high intensity exercise in the hea

129 sensitive ROS impairs NO-dependent cutaneous vasodilatation during intense exercise.

130 suggesting attenuated ET-B receptor mediated vasodilatation during local skin warming compared to Con

131 t nitric oxide (NO) contributes to cutaneous vasodilatation during moderate (400 W of metabolic heat

132 smotic saline affects sweating and cutaneous vasodilatation during passive heating.

133 development of impaired coronary arteriolar vasodilatation during simultaneous high-fat feeding.

134 inhibition would attenuate reflex cutaneous vasodilatation during sustained dynamic exercise in youn

135 BaCl(2) eliminated vasodilatation during the first contraction at the moder

136 ndothelial signalling pathways for ascending vasodilatation ensure increased oxygen delivery to activ

137 This augmented vasodilatation exceeds that predicted by a simple sum of

138 bition of endothelium-dependent flow-induced vasodilatation (FIV) assayed in pressurized mesenteric a

139 helial dysfunction and reduced flow-mediated vasodilatation (FMVD).

140 al perfusion pressure with hyperemia-induced vasodilatation (fractional flow reserve [FFR] </=0.80).

141 nhibition were determined by quantifying the vasodilatation from rest to SS hypoxia, as well as by qu

142 bition of NO and PGs abolishes local hypoxic vasodilatation (from rest to SS hypoxia) in the forearm

143 /-3%CVC(max), P < 0.001) as was NO-dependent vasodilatation (HC: 43+/-5 vs. NC: 62+/-4%CVC(max), P <

144 We propose that the attenuated ET-1-induced vasodilatation in AE-PCOS is a consequence of androgen r

145 ET(B) R inhibition decreased ET-1-induced vasodilatation in AE-PCOS women (logED(50) , 0.64 +/- 0.

146 EFS caused vasodilatation in arteries constricted with 1 mum U46619

147 VEGF induced vasodilatation in arterioles pre-contracted with ET-1 wa

148 GF produced a potent concentration dependent vasodilatation in arterioles pre-contracted with ET-1.

149 on endothelium-independent and K(+) -induced vasodilatation in denuded arteries.

150 lood pressure measurements, and flow-induced vasodilatation in endothelial cell-specific CSE knockout

151 c statin treatment improves reflex cutaneous vasodilatation in formerly hypercholesterolaemic older a

152 % CVC(max), both P < 0.001) and NO-dependent vasodilatation in HC (BH(4): 74 +/- 3% CVC(max); combo 7

153 Attenuated reflex cutaneous vasodilatation in healthy human ageing is mediated by al

154 straint of endothelium-dependent NO-mediated vasodilatation in healthy humans.

155 levels of AMPK activation are necessary for vasodilatation in healthy pregnancy.

156 Further, impaired ACh-induced vasodilatation in HF-SED was normalized by apocynin or T

157 Flow-induced vasodilatation in human resistance arteries is also regu

158 king Kir channels also inhibits flow-induced vasodilatation in human subcutaneous adipose microvessel

159 stration of BH(4) would augment NO-dependent vasodilatation in hypercholesterolaemic human skin, whic

160 Losmapimod improves nitric oxide-mediated vasodilatation in hypercholesterolemic patients, which i

161 Bevacizumab inhibits VEGF-induced vasodilatation in pre-contracted arterioles.

162 tive skeletal muscle fibres could facilitate vasodilatation in proportion to the degree of muscle fib

163 on fraction, and cardiac output and elicited vasodilatation in rat in vivo.

164 h leads to activation of MasR and splanchnic vasodilatation in rats.

165 g skeletal muscle have shown that functional vasodilatation in resistance arterioles has an endotheli

166 Reflex vasodilatation in response to a 1.0 degrees C rise in or

167 ts point to EC Kir channels as amplifiers of vasodilatation in response to increases in EC calcium an

168 Functional vasodilatation in response to muscle contraction recover

169 Vasodilatation in response to pressure was significantly

170 Cutaneous vasodilatation in response to SNP was significantly blun

171 o demonstrate that ET-1 attenuates cutaneous vasodilatation in response to sodium nitroprusside, sugg

172 The renal vasodilatation in septic acute kidney injury may be due

173 ted the hypotheses that (1) the compensatory vasodilatation in skeletal muscle during hypoxic exercis

174 e hypoxia has been demonstrated to result in vasodilatation in the coronary, cerebral, splanchnic and

175 nally examine the mechanisms of H2 S-induced vasodilatation in the human cutaneous microcirculation.

176 nuated the FPP-induced augmentation of rapid vasodilatation in the young (control: 1.25 +/- 0.23; L -

177 FPP increases the role of NO in PLM-induced vasodilatation in the young, but not the old, due to red

178 network in hypoxia is supported by increased vasodilatation in these regions to a subsequent hypercap

179 ensory-motor nerves have been shown to cause vasodilatation in vitro.

180 uced sympathetic activation elicits coronary vasodilatation in young adults that is impaired with adv

181 ribute to the prostacyclin-induced cutaneous vasodilatation in young males, these contributions are d

182 contribute to prostacyclin-induced cutaneous vasodilatation in young males, these contributions are d

183 rgic blockade abolished CPT-induced coronary vasodilatation in young men ( -33 +/- 6% vs. 0 +/- 6%, p

184 acetylcholine (ACh)-induced and flow-induced vasodilatations in isolated, pressurized coronary arteri

185 Endothelial cell-dependent vasodilatations in response to activation of muscarinic

186 Endothelium-dependent vasodilatations in response to muscarinic receptor, TRPV

187 PCOS may reflect lower endothelial-mediated vasodilatation independent of generally lower vascular r

188 hIGFBP1 induced vasodilatation independently of IGF and increased endoth

189 Delayed recovery of functional vasodilatation indicates that additional time is require

190 of N-cadherin AJ density at 50 mmHg, whereas vasodilatation induced by ACh (10(-5) m) was accompanied

191 ibited the increase in endothelium-dependent vasodilatation induced by nor-NOHA.

192 ABSTRACT: In response to exercise, vasodilatation initiated within the microcirculation of

193 Because cutaneous vasodilatation is a cardinal sign of a hot flush, these

194 thesized that impaired endothelium-dependent vasodilatation is a predictor of mortality in critically

195 bedside assessment of endothelium-dependent vasodilatation is an independent predictor of mortality

196 ated muscle contraction-dependent arteriolar vasodilatation is coupled through an endothelial cell-de

197 We demonstrate that reflex cutaneous vasodilatation is impaired in older hypercholesterolaemi

198 riment was to determine whether ATP-mediated vasodilatation is independent of nitric oxide (NO) and p

199 Thus, we conclude that ECM FN-dependent vasodilatation is mediated by the heparin-binding (RWRPK

200 ionally, we show that H2 S-induced cutaneous vasodilatation is mediated, in part, by tetraethylammoni

201 ffect in the old, but whether this augmented vasodilatation is nitric oxide (NO) dependent is unknown

202 els, but their role in endothelium-dependent vasodilatation is not clear.

203 elial cells (ECs) their role in EC-dependent vasodilatation is not clear.

204 Nitric oxide (NO)-dependent cutaneous vasodilatation is reportedly diminished during exercise

205 e that the primary mechanism of ATP-mediated vasodilatation is vascular hyperpolarization via activat

206 , consisting of vasoconstriction followed by vasodilatation, is critical for protecting the cutaneous

207 ase and stimulation of endothelium-dependent vasodilatation may explain impairments in both local vas

208 Exogenous H2 S elicits cutaneous vasodilatation mediated by KCa channels and has a functi

209 define the mechanisms mediating H2 S-induced vasodilatation, microdialysis fibres were perfused with

210 hibit K(IR) channels) abolished KCl-mediated vasodilatation (n = 6; %FVC = 134 +/- 13 vs. 4 +/- 5%; P

211 .05) and associated with markers of systemic vasodilatation (nitric oxide, rho = -0.66, P = 0.06; dia

212 endent (% Hyper) and endothelium-independent vasodilatation (% Nitro).

213 rfused in all sites to quantify NO-dependent vasodilatation (NO).

214 mechanisms responsible for the compensatory vasodilatation observed during hypoxic exercise in human

215 CPT decreased CVR (i.e. coronary vasodilatation occurred) in young ( -33 +/- 6%), but not

216 In contrast to the reflex vasodilatation occurring in response to stimulation of b

217 Similar to exercise, ATP-mediated vasodilatation occurs via activation of inwardly rectify

218 GP-EE induced endothelium- and NO-dependent vasodilatation of both rat aorta and small mesenteric ar

219 his dysfunction is attributable to a reduced vasodilatation of intracerebral arterioles and is revers

220 vation of extracellular K(+) to 14 mm caused vasodilatation of pressurized arteries, which was preven

221 Exposure to acute hypoxia results in vasodilatation of resistance arteries, as well as recrui

222 dea that Kir channels boost the EC-dependent vasodilatation of resistance-sized arteries.

223 intima-media thickness (IMT), flow-mediated vasodilatation of the brachial artery by ultrasound, ass

224 liminated ROV in the FA along with conducted vasodilatation of the FA initiated on the arteriole usin

225 the actions of nitric oxide, which leads to vasodilatation of the uterine vessels and might improve

226 GluR agonist, t-ACPD (100 muM), resulting in vasodilatations of 33.6+/-4.7% and 38.6+/-4.6%, respecti

227 ecent evidence suggests that beta-adrenergic vasodilatation offsets the vasoconstrictor effects of al

228 erate fall in cardiac output with coincident vasodilatation or a marked fall in cardiac output with n

229 on and triple blockade blunted Na2 S-induced vasodilatation (P < 0.05), whereas KATP and intermediate

230 ells in vivo similarly limits dermal AVH and vasodilatation, providing evidence that endothelial PPAR

231 eassuringly, this is because of compensatory vasodilatation rather than reduction in cardiac function

232 P<0.001), and was associated with increased vasodilatation, reduced thrombus formation, and an incre

233 ignalling mechanisms underlying ATP-mediated vasodilatation remain unclear.

234 dominantly IK/SK channel- and eNOS-dependent vasodilatation, respectively.

235 otion) and physiologic (i.e., thermogenesis, vasodilatation) responses.

236 brief tetanic contraction evoked rapid onset vasodilatation (ROV) (<1 s) throughout the resistance ne

237 ction (100 Hz for 500 ms) evoked rapid onset vasodilatation (ROV) in FAs that peaked within 4 s.

238 Rapid onset vasodilatation (ROV) in skeletal muscle is attenuated du

239 Rapid onset vasodilatation (ROV) initiates functional hyperaemia upo

240 thmic twitch contractions (4 Hz), slow onset vasodilatation (SOV) of FAs began after approximately 10

241 training attenuates the changes in cutaneous vasodilatation, sweat rate and cerebral blood flow durin

242 verity and within-flush changes in cutaneous vasodilatation, sweating and cerebral blood flow.

243 orespiratory fitness and attenuate cutaneous vasodilatation, sweating and the reductions in cerebral

244 TRACT: Exercise and intravascular ATP elicit vasodilatation that is dependent on activation of inward

245 underlies smooth muscle cell relaxation and vasodilatation, thereby increasing tissue blood flow and

246 We show that ET-1 attenuates cutaneous vasodilatation through a NOS-independent mechanism, poss

247 -1 attenuates methacholine-induced cutaneous vasodilatation through a NOS-independent mechanism.

248 genous glycine promotes sleep via peripheral vasodilatation through the activation of NMDA receptors

249 not mediate sweating, it modulates cutaneous vasodilatation to a similar extent in young and older ma

250 Vasodilatation to ACh and vasoconstriction to phenylephr

251 ow, the specific contribution of cholinergic vasodilatation to cerebral autoregulation remains unknow

252 Across branch orders, functional vasodilatation to single tetanic contraction (100 Hz, 50

253 e littermates resulting in impaired hindlimb vasodilatation to the ACE substrate, bradykinin.

254 lays a key role in coupling the magnitude of vasodilatation to the degree of contractile activity.

255 d that skeletal muscle contraction amplifies vasodilatation to the endothelium-dependent agonist ACh,

256 Endothelial-dependent vasodilatation, typically attenuated with age, was stron

257 OHA markedly increased endothelium-dependent vasodilatation (up to 2-fold) in patients with CAD+Diabe

258 An endothelium-dependent vasodilatation value of 0.5% or less predicted intensive

259 t the signalling events underlying ascending vasodilatation variy with the intensity and duration of

260 vasopressor that may mitigate sepsis-induced vasodilatation, vascular leakage, and edema, with fewer

261 selectively amplifies endothelium-dependent vasodilatation via activation of K(IR) channels.

262 K(+) (Kir2.1) channels regulate flow-induced vasodilatation via nitric oxide (NO) in mouse mesenteric

263 K(+) (Kir2.1) channels regulate flow-induced vasodilatation via nitric oxide (NO) in mouse mesenteric

264 42 degrees C heating, cutaneous NO-mediated vasodilatation was attenuated by 17.5%CVCmax (95% confid

265 Reflex vasodilatation was blunted in hypercholesterolaemic adul

266 Endothelium-dependent vasodilatation was calculated as the change in augmentat

267 imaging revealed that acetylcholine-mediated vasodilatation was impaired in cKO mice.

268 Endothelium-dependent vasodilatation was impaired in coronary arterioles from

269 Endothelium-dependent vasodilatation was impaired in high compared with normal

270 Maximal vasodilatation was increased by ~20-50% following 7 days

271 Carbachol-induced vasodilatation was increased in arteries from the RBP4-K

272 The vasodilatation was inhibited by 1 mum tetrodotoxin and 5

273 ek after stopping RIPC; however, NO-mediated vasodilatation was not affected by the RIPC stimulus.

274 sin II coinfusion, (Pyr(1))apelin-13-induced vasodilatation was preserved (P<0.02 for both).

275 Vasodilatation was reduced in hyperocholesterolaemic sub

276 Impaired EDHF-mediated vasodilatation was rescued by blocking G(i/o)alpha activ

277 altered, although the endothelium-dependent vasodilatation was severely impaired.

278 Endothelium-independent vasodilatation was slightly improved by nor-NOHA in the

279 c regression analysis, endothelium-dependent vasodilatation was the only predictor of mortality with

280 her the impairment in NO-dependent cutaneous vasodilatation was the result of a greater accumulation

281 the many metabolic signals that mediate this vasodilatation, we show here that the extracellular matr

282 helium-dependent and endothelium-independent vasodilatation were assessed with venous occlusion pleth

283 The plateau and NO-dependent vasodilatation were augmented in HC with arginase inhibi

284 sodilatation at the plateau and NO-dependent vasodilatation were reduced in HC subjects (plateau HC:

285 nolol at a concentration 1 mum inhibited the vasodilatation, whereas 0.1 mum of the beta(2) -adrenoce

286 s causes a large beta1-adrenoceptor-mediated vasodilatation, which contrasts with a smaller vasodilat

287 or appeared to be an enhanced eNOS-dependent vasodilatation, which was not liver-selective, as it was

288 supine bicycle exercise, and pharmacological vasodilatation with adenosine and acetylcholine.

289 e of effect of adropin-induced eNOS-mediated vasodilatation with advancing age.

290 be used to determine changes in NO-mediated vasodilatation with age, and thus, may be a clinically u

291 e (NO) to passive leg movement (PLM)-induced vasodilatation with age, with and without a posture-indu

292 e of effect of adropin-induced eNOS-mediated vasodilatation with ageing.

293 ifying potassium (K(IR) ) channels underlies vasodilatation with elevated muscle fibre recruitment wh

294 e that abnormal coronary vasomotion (reduced vasodilatation with exercise = reduced coronary flow res

295 volatile group showed a higher prevalence of vasodilatation with hypotension and higher cardiac outpu

296 activation is a key mechanism linking local vasodilatation with muscle fibre recruitment during exer

297 o determine the interaction of H2 S-mediated vasodilatation with nitric oxide (NO) and cyclo-oxygenas

298 ediates the NO component of reflex cutaneous vasodilatation with passive heat stress.

299 mediate NO synthesis during reflex cutaneous vasodilatation with sustained dynamic exercise.

300 Endothelial-dependent vasodilatation, with and without adropin incubation, was