ライフサイエンスコーパス: vasomotor

1 ertension and do not smoke manifest coronary vasomotor abnormalities.

2 However, its direct vasomotor action and its linkage to oxidative stress-ind

3 In this study, we directly assessed the vasomotor action of Ang II in isolated porcine coronary

4 t effect and the underlying mechanism of the vasomotor action of resveratrol were examined in retinal

5 t effect and the underlying mechanism of the vasomotor action of simvastatin in retinal arterioles wa

6 power; P < 0.001), indicative of sympathetic vasomotor activation.

7 bined an unbiased longitudinal assessment of vasomotor activity along a genetically defined vascular

8 functional connectivity arise from residual vasomotor activity as well as arteriole dynamics driven

9 Thus, the curcumin vasomotor activity on microcirculation was alpha-Ad and

10 mits chronic activation of basal sympathetic vasomotor activity under this condition.

11 ed and the signaling pathway underlying this vasomotor activity was probed.

12 re considered the main central generators of vasomotor activity.

13 les of neurons in baroreceptor regulation of vasomotor activity.

14 N-cadherin AJs are sensitive to pressure and vasomotor agonists in VSMCs and support a functional rol

15 d during changes in vascular tone induced by vasomotor agonists.

16 Hallmarks of the disease include vasomotor and cardiovascular instability and diminished

17 Six hours after exposure, vasomotor and fibrinolytic function were assessed by mea

18 ked impairment of PAR-1-mediated endothelial vasomotor and fibrinolytic function.

19 We compared RA and SV graft vasomotor and flow responses to endothelium-dependent an

20 rried, poorer physical functioning, and more vasomotor and gastrointestinal symptoms were significant

21 Significant dissociation of vasomotor and metabolic levodopa responses was seen in t

22 Vasomotor and musculoskeletal symptoms were similar betw

23 with significantly higher quality of life in vasomotor and other physical dimensions (all P <0.001).

24 estinal side effects were more frequent, and vasomotor and ovulatory symptoms less frequent, in the m

25 Symptoms were considered present with either vasomotor and/or joint complaints.

26 stane-treated patients with new or worsening vasomotor and/or joint symptoms would have improved RFS.

27 rves accompanied by impairment of sudomotor, vasomotor, and pilomotor function.

28 apsaicin leads to degeneration of sudomotor, vasomotor, and pilomotor nerves accompanied by impairmen

29 ght to determine if resetting of the carotid-vasomotor baroreflex function curve during exercise is m

30 wever, in comparison to control, the carotid-vasomotor baroreflex function curve was relocated downwa

31 We compared how vasomotor C neurons and secretomotor B neurons integrate

32 Taken together, these data suggest that vasomotor changes likely modulate extremity growth indir

33 docrine symptoms at trial entry was high for vasomotor complaints and sexual problems, which persiste

34 t the vascular endothelium was a key site of vasomotor control and that nitric oxide (NO) potentially

35 heavily dilated conduits that lack maternal vasomotor control but allow the placenta to meet an incr

36 tion of this balance contributes to impaired vasomotor control in diabetes.SIGNIFICANCE STATEMENT Ide

37 We tested the hypothesis that vasomotor control is differentially regulated between fe

38 We conclude that vasomotor control is differentially regulated in feed ar

39 s the hypothesis that peripheral sympathetic vasomotor control may operate by a direct mechanism (vas

40 Vasomotor control recovered at 21 days, when regenerated

41 ained ambiguous due to indirect estimates of vasomotor control.

42 istal extremities, in absence of sympathetic vasomotor denervation.

43 ime or another; specifically, 8% more in the vasomotor domain and 4% more each in the sexual domain a

44 Female patients have a higher prevalence of vasomotor dysfunction (especially CMD) compared with mal

45 f ET-1-induced contraction in the setting of vasomotor dysfunction after cardiac surgery.

46 associated with mechanical, electrical, and vasomotor dysfunction and adverse outcomes.

47 de A effectively reversed HAART drug-induced vasomotor dysfunction and eNOS down-regulation.

48 Endothelial vasomotor dysfunction and markers of systemic inflammati

49 tivation of LOX-1 and CD32 may contribute to vasomotor dysfunction and proatherogenic actions of CRP,

50 have been attributed to menopause, but only vasomotor dysfunction and vaginal dryness are consistent

51 The findings implicate vasomotor dysfunction as a potential mechanism involved

52 Both pathways mediate vasomotor dysfunction by inducing vascular oxidative str

53 Trials of therapies for vasomotor dysfunction have shown improvements with oestr

54 the prevalence and clinical presentation of vasomotor dysfunction in a European population and to ex

55 Perfusion defects may be caused by coronary vasomotor dysfunction in addition to atherosclerotic pla

56 Coronary vasomotor dysfunction is an important mechanism for angi

57 Vasomotor dysfunction is frequent in patients with angin

58 ts were more sensitive to acetylcholine with vasomotor dysfunction occurring at lower ACH doses compa

59 We hypothesized that vasomotor dysfunction of the coronary microcirculation i

60 diesel exhaust did not aggravate preexisting vasomotor dysfunction, but it did reduce the acute relea

61 s are all products of hemolysis that promote vasomotor dysfunction, proliferative vasculopathy, and a

62 or the management of myocardial dysfunction, vasomotor dysfunction, pulmonary hypertension, and right

63 and AZT-induced down-regulation of eNOS and vasomotor dysfunction.

64 rt, to endothelial dysfunction, particularly vasomotor dysregulation.

65 e studies should explore the contribution of vasomotor effects.

66 ion of NGF, the recovery of secretomotor and vasomotor efferents was determined by recording salivary

67 hemical analyses of pericytes, the capillary vasomotor elements.

68 Vascular and vasomotor events do not persist post-treatment across al

69 Fatigue, loss of sexual interest, and vasomotor flushing were less common in the bicalutamide

70 Deficits in vasomotor function and metabolic signature observed in A

71 promotes endothelial quiescence and governs vasomotor function and proportional remodeling of blood

72 d antioxidant therapies may favorably affect vasomotor function and thereby improve ischemia.

73 nvasive angiographic assessments of coronary vasomotor function have demonstrated an impairment of en

74 emic inflammation may contribute to impaired vasomotor function in forearm microvessels.

75 erse effects of CRP on endothelium-dependent vasomotor function in resistance arterioles.

76 e, that environmental manipulation of normal vasomotor function is capable of achieving therapeutical

77 hese findings provide evidence that coronary vasomotor function is impaired in patients with SLE and

78 ation at the single microvessel level on how vasomotor function is regulated in the human retina.

79 Loss of KV1.5 vasomotor function may play an important role in microva

80 Vasomotor function of aorta in vitro was examined 1 day

81 temic microinflammation and altered coronary vasomotor function of both the epicardial conductance an

82 ovement in coronary and brachial endothelial vasomotor function over six months.

83 AP-HSV showed impaired vasomotor function that was associated with increased ox

84 e its bioactivity and transduce an endocrine vasomotor function under certain conditions.

85 ric oxide-mediated and prostacyclin-mediated vasomotor function via LOX-1 activation.

86 Coronary vasomotor function was studied in response to cold press

87 een insulin resistance and abnormal coronary vasomotor function, a relationship that requires confirm

88 rve (CFR), an integrated measure of coronary vasomotor function, and to assess their contributions to

89 Endothelium-dependent vasomotor function, as measured by flow-mediated vasodil

90 portant determinant of endothelium-dependent vasomotor function.

91 esistant and exhibiting early restoration of vasomotor function.

92 sing noninvasive technique to study coronary vasomotor function.

93 al for proper capillary diameter control and vasomotor function.

94 test is a safe technique to assess coronary vasomotor function.

95 Vasomotor hot flashes are a common problem in menopausal

96 lete loss of vessel function; 4) CAA-induced vasomotor impairment resulted from dysfunction rather th

97 CAA formation and a decrease in CAA-induced vasomotor impairment.

98 influence vascular function is by affecting vasomotor innervation.

99 trogen action (uterotrophic, osteopenia, and vasomotor instability models) and yet were active in the

100 Symptoms of low T include decreased libido, vasomotor instability, and decreased bone mineral densit

101 es-spreading pain and skin hypersensitivity, vasomotor instability, osteopenia, edema, and abnormal s

102 verely reduce NO bioavailability and produce vasomotor instability.

103 action between MO-1 and the endothelial EDHF vasomotor mechanism that was reduced in the presence of

104 suggested to be a potential risk factor for vasomotor menopausal symptoms (VMSs), ie, hot flushes an

105 Symptomatic effects (eg, vasomotor, musculoskeletal) varied by medication.

106 thors speculate that functional disorders of vasomotor nerve cells, which originate in the embryonal

107 itatory preBotC neurons modulate sympathetic vasomotor neuron activity, generating heart rate and blo

108 on had no discernable effect on the putative vasomotor neurons at rest and was high enough to allow p

109 charge (PND) and putative sympathoexcitatory vasomotor neurons of the rostral ventrolateral medulla (

110 Absence of this regulation in vasomotor neurons suggests a different integrative funct

111 ss markers for cardiovascular presympathetic vasomotor neurons, respiratory propriobulbar rhythmogeni

112 ling with neuropeptide Y (NPY), a marker for vasomotor neurons, revealed selective cellular colocaliz

113 e relation between the reported incidence of vasomotor or joint symptoms and breast cancer recurrence

114 rmone-receptor-positive tumours who reported vasomotor or joint symptoms at the first follow-up visit

115 connected brain regions, entrain the ~0.1-Hz vasomotor oscillation in diameter of local arterioles.

116 duces long-lasting elevations in sympathetic vasomotor outflow and blood pressure in healthy humans.

117 ured as the relationship between sympathetic vasomotor outflow and either forearm vascular conductanc

118 MSNA operating point and resting sympathetic vasomotor outflow both are lower for highland Sherpa com

119 vascular responses to increasing sympathetic vasomotor outflow, termed sympathetic neurovascular tran

120 Disrupting supraspinal vasomotor pathways affects basal hemodynamics and contri

121 euronal tracing showed that host supraspinal vasomotor pathways regenerated into the graft, and 5-HT(

122 IFICANCE STATEMENT Disruption of supraspinal vasomotor pathways results in cardiovascular dysfunction

123 c symptoms and higher quality of life in the vasomotor, physical, and psychosocial dimensions (P < .0

124 There were reductions in sudomotor, vasomotor, pilomotor, and sensory function in capsaicin-

125 months with serial assessments of sudomotor, vasomotor, pilomotor, and sensory function with simultan

126 There were reductions in sudomotor, vasomotor, pilomotor, and sensory nerve fiber densities

127 e effects of exercise training on adrenergic vasomotor properties could contribute to the beneficial

128 Circulating ATP possesses unique vasomotor properties in humans and has been hypothesized

129 mans in vivo and may help explain the unique vasomotor properties of intravascular ATP in the human c

130 determine the effect of exercise training on vasomotor properties of isolated peripheral collateral a

131 t both direct (parenchymatous) and indirect (vasomotor) protective mechanisms.

132 tients with high-grade stenosis and impaired vasomotor reactivity (VMR) but no stroke.

133 us the Xience metallic stent in angiographic vasomotor reactivity after administration of intracorona

134 nship between coronary endothelium-dependent vasomotor reactivity and atheroma volume remains constan

135 ot meet its co-primary endpoints of superior vasomotor reactivity and non-inferior late luminal loss

136 The vasomotor reactivity at 3 years was not statistically di

137 artery endothelial function, as assessed by vasomotor reactivity during isometric handgrip exercise

138 teral hemispheric hypoperfusion and impaired vasomotor reactivity from critical internal carotid or m

139 strating a significant decrease (P < .05) in vasomotor reactivity in the treated group.

140 9-.98, p = .032), whereas decreased baseline vasomotor reactivity predicted incident depressive disor

141 le cerebral artery blood flow velocities and vasomotor reactivity were measured with transcranial Dop

142 Reduced vasomotor reactivity, which might indicate cerebral micr

143 sensitive K+ channels (K(ATP)) contribute to vasomotor regulation in some species.

144 ors linking to deleterious actions of CRP in vasomotor regulation remains unknown.

145 pport a functional role of N-cadherin AJs in vasomotor regulation.

146 mportant role in nitric oxide (NO)-dependent vasomotor regulation.

147 y vascular endothelium is a newly identified vasomotor-regulatory mechanism also involved in molecula

148 nce is dependent on the degree of neural and vasomotor reserve available for vasoconstriction.

149 Rac1 is essential for endothelium-dependent vasomotor response and ischemia-induced angiogenesis.

150 ly reduced propagation but not initiation of vasomotor response in the nondiabetic retina.

151 Besides, endothelial-dependent vasomotor response to acetylcholine (ie, endothelial fun

152 In women in this study, impaired coronary vasomotor response to acetylcholine was independently li

153 molecular mechanisms implicated in cutaneous vasomotor response to cooling are emerging from recent l

154 cident with this suprahyperpolarization, the vasomotor response to hypoxia is fundamentally altered.

155 SES, MgBRS demonstrated a higher capacity of vasomotor response to pharmacological agents (either end

156 ascular diameter control, and propagation of vasomotor response were diminished in diabetic retinas f

157 stimulation of a pericyte produced a robust vasomotor response, which propagated along the blood ves

158 ate the spatial and temporal dynamics of the vasomotor response.

159 F improved NO-mediated endothelium-dependent vasomotor responses and reduced vascular superoxide, bot

160 expressed peptides in the CNS, also produces vasomotor responses by inducing calcium release from int

161 connexin40 knockout (Cx40-/-) mice to study vasomotor responses induced by 10-second trains of elect

162 ol, we investigated network architecture and vasomotor responses of arterioles in the gluteus maximus

163 in-converting enzyme (ECE)-1 in ET-1-induced vasomotor responses of single retinal arterioles.

164 Endothelial-dependent vasomotor responses showed vasoconstriction of the arter

165 ular superoxide/peroxynitrite production and vasomotor responses to acetylcholine and bradykinin were

166 ed plasma and vascular levels of biopterins, vasomotor responses to acetylcholine, and vascular super

167 Recovery of tone and vasomotor responses to agonists occur in concert with my

168 flow reserve, microvascular resistance, and vasomotor responses to intracoronary acetylcholine (vaso

169 In heart failure subjects, vasomotor responses to isometric handgrip and cold press

170 53 mm Hg in the ex vivo retina did not alter vasomotor responses, indicating that although O(2) can m

171 ammation, and improved endothelium-dependent vasomotor responses.

172 nsory nerves with capsaicin had no effect on vasomotor responses.

173 This is crucial for coordinated vasomotor responses.

174 However, an intrinsic impairment of vasomotor responsiveness and sympathetic baroreflex func

175 Serum apoAI was associated with increased vasomotor responsiveness to ACh and flickering light and

176 ctomy had been applied mainly in intractable vasomotor rhinitis and severe perennial allergic rhiniti

177 such as in so-called idiopathic (previously 'vasomotor') rhinitis.

178 ced a clinically meaningful worsening in the vasomotor, sexual, physical, and psychosocial domains of

179 latory capacity of cerebral arterioles for a vasomotor stimulus for maintaining a spontaneous and ins

180 lation of the brachial artery in vivo and by vasomotor studies in saphenous vein segments ex vivo.

181 l arterioles (~50-100 mum) were isolated for vasomotor study and molecular assessment of ROCK isoform

182 nsitivity during orthostasis, though upright vasomotor sympathetic activity is not clearly different

183 Vasomotor sympathetic activity plays an important role i

184 revealed the presence of VMAT2-positive, non-vasomotor sympathetic axons in the submandibular gland a

185 s post-I activity in laryngeal adductors and vasomotor sympathetic nerves and interacts with other me

186 min) orthostasis without obvious changes in vasomotor sympathetic neural control.

187 dering short-term use of hormone therapy for vasomotor symptom relief in such women.

188 ne whether gains in body fat were related to vasomotor symptom reporting over time.

189 standard" for comparison with retrospective vasomotor symptom reporting.

190 symptoms per day, symptom intensity, Wiklund Vasomotor Symptom Subscale score did not differ between

191 mptoms (1 = mild to 3 = severe), and Wiklund Vasomotor Symptom Subscale.

192 necological problems (0.29 vs 0.19, P<.001), vasomotor symptoms (0.96 vs 0.85, P<.001), leg cramps (1

193 Rate and intensity of vasomotor symptoms (1 = mild to 3 = severe), and Wiklund

194 Vasomotor symptoms (1.33 vs 1.17; p=0.011), difficulty w

195 nd mental health component scale scores, and vasomotor symptoms (as per the BCPT symptom scale).

196 Assessments also included reported vasomotor symptoms (hot flashes, night sweats) and serum

197 Although most women report vasomotor symptoms (hot flashes, night sweats) during mi

198 as significantly associated with more severe vasomotor symptoms (mean severity score 1.45 for age <60

199 associated with increased odds of reporting vasomotor symptoms (per standard deviation increase in p

200 of life (HRQOL) during midlife in women when vasomotor symptoms (VMS) and sleep disturbance commonly

201 survival outcomes and specific AEs including vasomotor symptoms (VMSs), musculoskeletal adverse event

202 depressive, anxiety, sleep disturbance, and vasomotor symptoms and menopause transition stages.

203 led trial tested whether acupuncture reduces vasomotor symptoms and produces fewer adverse effects th

204 t base line, estrogen and progestin improved vasomotor symptoms and resulted in a small benefit in te

205 Vasomotor symptoms and sexual dysfunction occur frequent

206 Vasomotor symptoms are common adverse effects of antiest

207 e treatment of major depressive disorder and vasomotor symptoms associated with menopause.

208 0 to 54 years of age with moderate-to-severe vasomotor symptoms at base line, estrogen and progestin

209 Presence of vasomotor symptoms at baseline was ascertained from a 34

210 Women gave detailed information on any vasomotor symptoms at each 6-month follow-up visit.

211 7.5%) eligible women reported newly emergent vasomotor symptoms at the 3-month follow-up visit and ha

212 Body fat change was examined in relation to vasomotor symptoms by using generalized estimating equat

213 Body fat is positively associated with vasomotor symptoms cross-sectionally, but the longitudin

214 depressive, anxiety, sleep disturbance, and vasomotor symptoms did not account for the transient dec

215 adiposity would be associated with decreased vasomotor symptoms during menopause because of conversio

216 0% had over 63 hot flashes/week, and 75% had vasomotor symptoms for >or= 6 months.

217 est acupuncture may be effective in reducing vasomotor symptoms in menopausal women.

218 assessments and higher among women reporting vasomotor symptoms in the daily assessment on the day of

219 ors examined the relation of such factors to vasomotor symptoms in the multiethnic sample of 3,302 wo

220 ting accuracy, which was relatively high for vasomotor symptoms in this study.

221 nal relation between changes in body fat and vasomotor symptoms is uncharacterized.

222 The reduction in vasomotor symptoms must be weighed against other risks a

223 The appearance of new vasomotor symptoms or joint symptoms within the first 3

224 The difference in vasomotor symptoms per day between placebo and any of th

225 es between treatment groups smaller than 1.5 Vasomotor symptoms per day cannot be ruled out.

226 for hormone therapy versus placebo was -4.06 vasomotor symptoms per day for the average over all the

227 Vasomotor symptoms per day, symptom intensity, Wiklund V

228 351 women age 45 to 55 years with 2 or more vasomotor symptoms per day; 52% of the women were in men

229 a safe, effective and durable treatment for vasomotor symptoms secondary to long-term antiestrogen h

230 nd specificity of retrospective reporting of vasomotor symptoms using data from 567 participants in t

231 ecificity for retrospective reporting of any vasomotor symptoms versus none in the past 2 weeks.

232 ody fat, reproductive hormones, and reported vasomotor symptoms were assessed annually over 4 years f

233 Vasomotor symptoms were evaluated according to follow-up

234 MA significantly reduced vasomotor symptoms with durable benefit over 6 months.

235 of hormone therapy that can be used to treat vasomotor symptoms without increasing the risk of stroke

236 age were also significantly associated with vasomotor symptoms, although a dose-response relation wi

237 spasm, gynaecological cancers and symptoms, vasomotor symptoms, and deep vein thromboses with tamoxi

238 therapy is recommended only for treatment of vasomotor symptoms, and some formulations might be safer

239 on-life-threatening adverse effects, such as vasomotor symptoms, have an important influence in its u

240 group reported more gynecological problems, vasomotor symptoms, leg cramps, and bladder control prob

241 ll negative effects on women's self-reported vasomotor symptoms, sexual symptoms, and pain, which occ

242 Less education, being Hispanic, and vasomotor symptoms, stressful life events, and low socia

243 ts and survivors use black cohosh to relieve vasomotor symptoms, there is limited information on its

244 ether other factors, such as the presence of vasomotor symptoms, use of hormone therapy, and the occu

245 ents younger than 35 years receiving OFS was vasomotor symptoms, with the greatest worsening from bas

246 findings support a thermoregulatory model of vasomotor symptoms.

247 d be associated with a greater likelihood of vasomotor symptoms.

248 Herbal supplements are widely used for vasomotor symptoms.

249 ential as an important therapy for relief of vasomotor symptoms.

250 somewhat greater in women with self-reported vasomotor symptoms.

251 r women with postgraduate education reported vasomotor symptoms.

252 nutrients were significantly associated with vasomotor symptoms.

253 e and Japanese than Caucasian women reported vasomotor symptoms.

254 tyle changes for women that may help prevent vasomotor symptoms.

255 e reserved for women with moderate to severe vasomotor symptoms.

256 with an overall decrease in the frequency of vasomotor symptoms.

257 luded decreased hip fractures, diabetes, and vasomotor symptoms.

258 of nerve storms and Peter Wallwork Latham's vasomotor theory, providing a detailed accounts of their

259 s associated with a reduction in sympathetic vasomotor tone (as revealed by frequency domain analysis

260 0.001), heart rate (P < 0.001), sympathetic vasomotor tone (P < 0.001) and the noradrenaline levels

261 This severe impairment of vasomotor tone after CTO reopening suggests that intraco

262 bition significantly reduces the sympathetic vasomotor tone and augments the sympathoinhibitory respo

263 olateral medulla (RVLM) maintain sympathetic vasomotor tone and blood pressure through their direct e

264 SRF-related decreases in vasomotor tone and cell-matrix attachment increase arter

265 helial cell (EC) apoptosis predicts abnormal vasomotor tone and contributes to circulating tissue fac

266 ng intravascular hemolysis in human disease, vasomotor tone and organ perfusion may be impaired by th

267 logical actions that include regulating both vasomotor tone and renal sodium excretion.

268 pose tissue (PVAT)-derived factors influence vasomotor tone and the PVAT proteome in lean versus obes

269 These data suggest that alterations in vasomotor tone are the primary mechanism by which the CB

270 thelial transcytosis, vascular permeability, vasomotor tone control, and vascular reactivity.

271 Diminished vasomotor tone during the initial stages of regeneration

272 activity in the PVN and elevated sympathetic vasomotor tone in essential hypertension.

273 f PVN presympathetic neurons and sympathetic vasomotor tone in hypertension.

274 ritically involved in heightened sympathetic vasomotor tone in hypertension.

275 naptic NMDAR activity to elevate sympathetic vasomotor tone in hypertension.SIGNIFICANCE STATEMENT He

276 herapeutic approach for reducing sympathetic vasomotor tone in neurogenic hypertension.

277 sympathetic neurons and elevated sympathetic vasomotor tone in neurogenic hypertension.

278 he hypothalamus maintain resting sympathetic vasomotor tone in spontaneously hypertensive rats (SHR).

279 nally projecting PVN neurons and sympathetic vasomotor tone in spontaneously hypertensive rats (SHRs)

280 role of hydrogen sulfide (H2S) in regulating vasomotor tone in the fetoplacental vasculature.

281 IGNIFICANCE STATEMENT Heightened sympathetic vasomotor tone is a major contributor to the development

282 of SIRT1 in regulating endothelium-dependent vasomotor tone is not known.

283 Baroreflex-mediated changes in sympathetic vasomotor tone may have a limited acute effect on muscle

284 nt to which K(ATP) participate in regulating vasomotor tone under physiological and pathophysiologica

285 eral' capillary), is specialized to regulate vasomotor tone, and functions as a stem/progenitor cell

286 of that mechanism to endothelial control of vasomotor tone, angiogenesis, and/or inflammatory activa

287 r than nitric oxide (NO)-mediated control of vasomotor tone, are poorly characterized in patients wit

288 Spontaneous vasomotor tone, endothelium-dependent dilatation and adr

289 posure to low concentration of PM2.5 altered vasomotor tone, induced vascular inflammation, and poten

290 a central role in the regulation of arterial vasomotor tone, releasing nitric oxide for vasodilation.

291 siologic functions, including the control of vasomotor tone, the trafficking of cells and nutrients,

292 hanges in mean systemic filling pressure and vasomotor tone.

293 that FHL2 is essential for the regulation of vasomotor tone.

294 ed to Control by 21 days, as did spontaneous vasomotor tone.

295 dothelial cells and thereby the NO-dependent vasomotor tone.

296 , a hypercoaguable state, and alterations in vasomotor tone.

297 constrictors contributing to basal cutaneous vasomotor tone.

298 also by modulating the autonomic control of vasomotor tone.

299 n degradation, tissue factor expression, and vasomotor tone.

300 ed by miR-130/301, including those involving vasomotor tone.