ライフサイエンスコーパス: vasodilatation

1 uced a profound hypothermia due to cutaneous vasodilatation.

2 ression of exogenous H2 S-mediated cutaneous vasodilatation.

3 mune disorders, in the modulation of carotid vasodilatation.

4 Na2 S and NaHS elicited dose-dependent vasodilatation.

5 nitroprusside was perfused to elicit maximal vasodilatation.

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

7 on vascular permeability, angiogenesis, and vasodilatation.

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

9 ra-arterial blood pressure to quantify local vasodilatation.

10 cellular pathway that coordinates spreading vasodilatation.

11 ced vasoconstriction and hypercapnia-induced vasodilatation.

12 ults without parallel increases in cutaneous vasodilatation.

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

14 mutually required to elicit angiogenesis and vasodilatation.

15 unction resulting in impaired EDHF-dependent vasodilatation.

16 ood flow responses and endothelium-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 exposure, despite peripheral limitations to vasodilatation.

22 nces on vascular tone and thus isolate local vasodilatation.

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

24 on, but did not correlate with the prolonged vasodilatation.

25 motor unit recruitment and the initiation of vasodilatation.

26 microm) eliminated this ACh- or flow-induced vasodilatation.

27 al root reflexes (DRRs) to induce peripheral vasodilatation.

28 vidence that ADRB2 gene variation influences vasodilatation.

29 ous vasoconstriction followed by a prolonged vasodilatation.

30 nitroprusside was infused to achieve maximal vasodilatation.

31 ptors on the vascular smooth muscle to cause vasodilatation.

32 ) to an improvement in endothelium-dependent vasodilatation.

33 not depend on new synthesis of NO to produce vasodilatation.

34 nimal in comparison to the effects of muscle vasodilatation.

35 eceptors in dermal capillaries causing their vasodilatation.

36 ing no effect on beta2-mediated hindquarters vasodilatation.

37 onstriction while decreases in PO2 result in vasodilatation.

38 hyperpolarization and endothelium-dependent vasodilatation.

39 saline did not affect sweating or cutaneous vasodilatation.

40 such as angiogenesis, glucose tolerance, and vasodilatation.

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

42 /- 0.18 degrees C, P </= 0.01) and cutaneous vasodilatation (+1.15 +/- 0.18 vs. +1.53 +/- 0.22 degree

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

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

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

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

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

48 +/- 4% CVC(max), P < 0.001) and NO-dependent vasodilatation (68 +/- 3% CVC(max), P < 0.001).

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

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

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

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

53 ation significantly diminished NS309-induced vasodilatation and abolished substance P- or adenosine 5

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

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

56 nosine contributes to hypoxia-induced muscle vasodilatation and bradycardia by acting on A(1) recepto

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

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

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

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

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

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

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

64 ion in humans causes peripheral and coronary vasodilatation and increases cardiac output.

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

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

67 ring acute inflammatory process, with dermal vasodilatation and leukocyte infiltration as central fea

68 of age and chronic exercise on flow-induced vasodilatation and levels of NO and O(2)(-) in soleus mu

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

70 dicate that ET(B) receptors may provide both vasodilatation and neuroprotection.

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

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

73 diverse range of physiological effects, from vasodilatation and platelet disaggregation to synaptic p

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

90 (P2Y) on the endothelium evoking subsequent vasodilatation, and ageing is typically associated with

91 es, the potential role of nitrite in hypoxic vasodilatation, and an unexpected protective action of n

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

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

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

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

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

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

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

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

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

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

102 .9, 9.2; P = 0.03) and NO-mediated cutaneous vasodilatation at 42 degrees C heating by 19.6% CVCmax (

103 ic exercise hyperaemia and abolishes hypoxic vasodilatation at rest.

104 Vasodilatation at the plateau and NO-dependent vasodilat

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

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

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

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

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

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

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

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

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

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

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

116 injection of agitated saline (intrapulmonary vasodilatation); controls did not meet both criteria for

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 monstrate both cerebral vasoconstriction and vasodilatation, depending on the model and dose studied.

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

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

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

124 NO) contributes to augmented skeletal muscle vasodilatation during hypoxic exercise and (2) the combi

125 tor activation would attenuate the augmented vasodilatation during hypoxic exercise more than NO inhi

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

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

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

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

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

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

132 sms by which adenosine contributes to muscle vasodilatation during systemic hypoxia and exercise are

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

134 ion in a dose-dependent manner compared with vasodilatation evoked via adenosine.

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

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

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

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

139 scavenging with Tempol reduced flow-induced vasodilatation from all groups except young SED rats.

140 Catalase reduced flow-induced vasodilatation from all groups.

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 s to the age-related decline in flow-induced vasodilatation; however, reactive oxygen species are req

145 l-treated arterioles eliminated flow-induced vasodilatation in arterioles from all groups.

146 Exercise training enhanced flow-induced vasodilatation in arterioles from young and old rats.

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 esized that while the ET-B receptors mediate vasodilatation in both groups of women, this response wo

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

151 s, losartan restored impaired eNOS-dependent vasodilatation in diabetics.

152 adults, and aminophylline did not impact the vasodilatation in either group.

153 % CVC(max), both P < 0.001) and NO-dependent vasodilatation in HC (BH(4): 74 +/- 3% CVC(max); combo 7

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

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

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

157 xidative stress impair endothelium-dependent vasodilatation in humans, leading to the speculation tha

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

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

160 ine, and sodium nitroprusside caused forearm vasodilatation in patients and control subjects (all P<0

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

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

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

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

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

166 Cutaneous vasodilatation in response to SNP was significantly blun

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

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

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

170 oxygen species are required for flow-induced vasodilatation in soleus muscle arterioles from young an

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

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

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

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

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

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

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

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

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

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

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

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

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

184 hIGFBP1 induced vasodilatation independently of IGF and increased endoth

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

186 ding that these afferents were stimulated by vasodilatation induced by injection of vasoactive drugs.

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

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

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

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

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

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

193 vascular bed, whereas substance P-stimulated vasodilatation is eNOS mediated.

194 , we tested the hypothesis that ATP-mediated vasodilatation is impaired with age in healthy humans.

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

196 not reduced with age, and that ATP-mediated vasodilatation is independent of P1-receptor stimulation

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

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

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

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

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

202 r data also indicate that adenosine mediated vasodilatation is not reduced with age, and that ATP-med

203 Endothelium-dependent vasodilatation is reduced with advancing age in humans,

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 suggest that NO contributes to the augmented vasodilatation observed during hypoxic exercise independ

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

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

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

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

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

221 integrin-binding sequence produce sustained vasodilatation of rat skeletal muscle arterioles.

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

223 elated decline of nitric oxide (NO)-mediated vasodilatation of soleus muscle arterioles.

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

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

226 ads to progressive hypoxemia through diffuse vasodilatation of the pulmonary microcirculation.

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

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

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

230 ate the role of the skeletal muscle pump and vasodilatation on cardiovascular function during exercis

231 energic responsiveness.However, heat-induced vasodilatation opposes alpha-adrenergic vasoconstriction

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

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

234 metric contractions have been shown to limit vasodilatation, potentially leading to a greater mismatc

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

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

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

238 ignalling mechanisms underlying ATP-mediated vasodilatation remain unclear.

239 Endothelium-mediated vasodilatation responses were significantly greater to e

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

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

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

243 Rapid onset vasodilatation (ROV) initiates functional hyperaemia upo

244 contraction and produced rapid (<1 s) onset vasodilatation (ROV; diameter change, 10 +/- 1 mum) of t

245 thesis that ageing would impair 'rapid onset vasodilatation' (ROV) in distributing arterioles (second

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

247 requently precipitated by events that worsen vasodilatation, such as spontaneous bacterial peritoniti

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

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

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

251 iduals homozygous for Gly16 produces greater vasodilatation than those homozygous for Arg16.

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

253 To effect permanent vasodilatation, the internal elastic lamina and medial e

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

255 le weaker in strength and without associated vasodilatation, this response pattern is mimicked by gen

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

257 -1 attenuates methacholine-induced cutaneous vasodilatation through a NOS-independent mechanism.

258 otes vasoconstriction and inhibits ascending vasodilatation through activating alpha-adrenoreceptors.

259 (NO) from endothelium is a major mediator of vasodilatation through cGMP/PKG signals that lead to a d

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

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

262 Vasodilatation to acetylcholine (P=0.01) but not apelin

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

264 Vasodilatation to local heating, a NO-dependent response

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

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

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

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

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

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

271 Flow-induced vasodilatation was assessed under control conditions and

272 42 degrees C heating, cutaneous NO-mediated vasodilatation was attenuated by 17.5%CVCmax (95% confid

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

274 NO-mediated vasodilatation was examined in young, older sedentary an

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

276 Endothelium-dependent vasodilatation was impaired in coronary arterioles from

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

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

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

280 Vasodilatation was reduced in hyperocholesterolaemic sub

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

282 In Tempol-treated arterioles, flow-induced vasodilatation was restored by deferoxamine, an iron che

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

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

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

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

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

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

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

290 (PE; 1 x 10(9)-1 x 10(4)m), and flow-induced vasodilatation were determined.

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

292 rritory demonstrated preserved flow-mediated vasodilatation, whereas SV grafts did not.

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

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

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

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

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

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

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

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