ライフサイエンスコーパス: vasomotor

1 ertension and do not smoke manifest coronary vasomotor abnormalities.

2 ct or rather a more general endothelial cell vasomotor abnormality.

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

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

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

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

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

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

9 These data indicate that alterations in vasomotor activity are the primary means by which the ca

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

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

12 ual touch, muscular and visceral sensations, vasomotor activity, hunger, thirst, and 'air hunger'.

13 re considered the main central generators of vasomotor activity.

14 les of neurons in baroreceptor regulation of vasomotor activity.

15 channel is a critical regulator of episodic vasomotor activity.

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

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

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

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

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

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

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

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

24 Vasomotor and musculoskeletal symptoms were similar betw

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

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

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

28 tion in arterial pressure may be mediated by vasomotor and/or renal mechanisms.

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

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

31 clude the removal of heart, respiration, and vasomotor artifacts, a dramatic increase in spatial reso

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

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

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

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

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

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

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

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

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

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

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

43 ained ambiguous due to indirect estimates of vasomotor control.

44 istal extremities, in absence of sympathetic vasomotor denervation.

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

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

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

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

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

50 Endothelial vasomotor dysfunction and markers of systemic inflammati

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

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

53 The findings implicate vasomotor dysfunction as a potential mechanism involved

54 Both pathways mediate vasomotor dysfunction by inducing vascular oxidative str

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

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

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

58 Coronary vasomotor dysfunction is an important mechanism for angi

59 Vasomotor dysfunction is frequent in patients with angin

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

61 We hypothesized that vasomotor dysfunction of the coronary microcirculation i

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

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

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

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

66 rt, to endothelial dysfunction, particularly vasomotor dysregulation.

67 e studies should explore the contribution of vasomotor effects.

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

69 hemical analyses of pericytes, the capillary vasomotor elements.

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

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

72 Deficits in vasomotor function and metabolic signature observed in A

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

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

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

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

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

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

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

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

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

82 Vasomotor function of aorta in vitro was examined 1 day

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

84 represents a time-related improvement in the vasomotor function of the RA, which could have implicati

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

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

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

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

89 Coronary vasomotor function was studied in response to cold press

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

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

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

93 es have shown impaired endothelium-dependent vasomotor function, the effects of inflammation on the e

94 onography of the brachial artery to evaluate vasomotor function, with guidelines for its research app

95 portant determinant of endothelium-dependent vasomotor function.

96 al for proper capillary diameter control and vasomotor function.

97 sing noninvasive technique to study coronary vasomotor function.

98 ases (MAPK) have been implicated in coronary vasomotor function.

99 inimal lesions), we examined O2*- levels and vasomotor function.

100 ation that can be quantitated as an index of vasomotor function.

101 rosclerosis may contribute to improvement in vasomotor function.

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

103 Vasomotor hot flashes are a common problem in menopausal

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

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

106 influence vascular function is by affecting vasomotor innervation.

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

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

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

110 verely reduce NO bioavailability and produce vasomotor instability.

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

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

113 tagonist altered the ongoing activity of the vasomotor neurones.

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

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

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

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

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

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

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

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

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

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

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

125 In seven barbiturate-anesthetized rats, 16 vasomotor presympathetic neurons were filled with biotin

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

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

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

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

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

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

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

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

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

135 The vasomotor reactivity at 3 years was not statistically di

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

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

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

139 9-.98, p = .032), whereas decreased baseline vasomotor reactivity predicted incident depressive disor

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

141 Reduced vasomotor reactivity, which might indicate cerebral micr

142 quires either CC or EPR to reset the carotid-vasomotor reflex.

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

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

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

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

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

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

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

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

159 d dilatation to acetylcholine (ACh), whereas vasomotor responses in arteries transduced with S1179AeN

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

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

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

163 Endothelial-dependent vasomotor responses showed vasoconstriction of the arter

164 a short segment of arteriole is stimulated, vasomotor responses spread bidirectionally along the ves

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

168 53 mm Hg in the ex vivo retina did not alter vasomotor responses, indicating that although O(2) can m

169 ammation, and improved endothelium-dependent vasomotor responses.

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

171 This is crucial for coordinated vasomotor responses.

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

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

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

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

176 oth sympathetic nerve activity and intrinsic vasomotor rhythmicity; and (4) the dynamic relationship

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

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

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

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

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

182 Vasomotor sympathetic activity plays an important role i

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

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

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

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

187 standard" for comparison with retrospective vasomotor symptom reporting.

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

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

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

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

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

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

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

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

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

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

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

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

200 strogens for treatment of moderate-to-severe vasomotor symptoms and for prevention of osteoporosis.

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

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

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

204 Vasomotor symptoms and sexual dysfunction occur frequent

205 th medroxyprogesterone acetate (MPA) improve vasomotor symptoms and vaginal atrophy, provide acceptab

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 Both women and men experiencing vasomotor symptoms should be offered interventions for s

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

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

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

234 Vasomotor symptoms were evaluated according to follow-up

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

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

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

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

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

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

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

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

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

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

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

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

247 findings support a thermoregulatory model of vasomotor symptoms.

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

249 Herbal supplements are widely used for vasomotor symptoms.

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

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

252 r women with postgraduate education reported vasomotor symptoms.

253 nutrients were significantly associated with vasomotor symptoms.

254 e and Japanese than Caucasian women reported vasomotor symptoms.

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

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

257 t therapy, follicle-stimulating hormone, and vasomotor symptoms.

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

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

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

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

262 0.001), heart rate (P < 0.001), sympathetic vasomotor tone (P < 0.001) and the noradrenaline levels

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

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

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

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

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

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

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

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

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

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

273 our understanding of sympathetic control of vasomotor tone during exercise, we employed a technique

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

275 ritically involved in heightened sympathetic vasomotor tone in hypertension.

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

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

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

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

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

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

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

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

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

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

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

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

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

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 that FHL2 is essential for the regulation of vasomotor tone.

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

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

295 constrictors contributing to basal cutaneous vasomotor tone.

296 also by modulating the autonomic control of vasomotor tone.

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

298 blood vessels affecting cardiac function and vasomotor tone.

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

300 hanges in mean systemic filling pressure and vasomotor tone.