ライフサイエンスコーパス: vascular

1 Pulmonary vascular abnormalities such as vessel enlargement and re

2 ewed by 2 authors for characteristic retinal vascular abnormalities.

3 nous fistulas placed surgically for dialysis vascular access have a high primary failure rate resulti

4 Objective: To determine if vascular aging before the induction of hyperlipidemia en

5 lating progeronic and antigeronic factors in vascular aging is discussed.

6 Third-party vascular allografts (VAs) are an invaluable resource in

7 ed by dysregulated angiogenesis and impaired vascular and alveolar development.

8 be associated with oxidative stress-induced vascular and brain damage, mediated by activation of the

9 The presence of methanogens in vascular and cardiac tissues was assessed by indirect im

10 tion typically precedes the onset of retinal vascular and even some neurodegenerative diseases, the a

11 chips and the repeated sampling of both the vascular and interstitial compartments without compromis

12 ctions in cerebral soluble amyloid-beta1-42, vascular and parenchymal amyloid-beta deposits, and astr

13 neuroendocrine (NE) cancers, such as highly vascular and red/purple tumor lesions, spindle-shaped ce

14 al amyloid angiopathy (CAA) are two distinct vascular angiopathies that share several similarities in

15 ucts with complex and heterogeneous internal vascular architectures.

16 ascular microglia at all ages associate with vascular areas void of astrocyte endfeet, and the develo

17 and antiaging interventions, with a focus on vascular aspects of the aging process and its cardiovasc

18 of white blood cells (WBCs) in the pulmonary vascular bed is crucial for an effective immune response

19 s - and in some cases no polymer (to improve vascular biocompatibility) - and new antiproliferative d

20 This novel bioassay has usefulness in vascular biology research, patient phenotyping, drug tes

21 with magnetic resonance imaging findings of vascular brain injury or cerebral atrophy in adult Ameri

22 lial and neuronal nitric oxide synthase, and vascular/brain infiltration with inflammatory cells.

23 MAP20 is expressed during the late stages of vascular bundle development and localizes around forming

24 aging technologies allow analysis of retinal vascular caliber beyond the standard areas surrounding t

25 ese results uncover a major cause of hepatic vascular cavernomas and provide a road map for their per

26 Single-cell RNA sequencing of vascular cells in mice suggested that the vast majority

27 nants of induced transcriptional programs in vascular cells, like endothelial cells and vascular smoo

28 d endothelial cells-the two major classes of vascular cells.

29 oof of concept for understanding age-related vascular changes and imply that therapeutic targeting of

30 Vascular comorbidities have a deleterious impact on mult

31 ular complex, and microaneurysms in the deep vascular complex (DVC) (p = 0.003, 0.013, 0.028, 0.003,

32 llary density (NFLP_CD), macular superficial vascular complex vessel density (mSVC_VD), and foveal av

33 on number, microaneurysms in the superficial vascular complex, and microaneurysms in the deep vascula

34 Of these, 9.3% (n=3257) experienced a vascular complication while 7.6% (n=2651) had an in-hosp

35 Rates of both vascular complications and bleeding events decreased ove

36 The primary outcomes were in-hospital vascular complications and bleeding events.

37 Two-thousand three-hundred forty-seven vascular complications in 6,124 venoarterial extracorpor

38 inflammation is a feature of diabetes-driven vascular complications, in particular activation of the

39 ising strategy for the treatment of diabetic vascular complications.

40 pective of periprocedural major bleeding and vascular complications.

41 ogical and immunohistochemical review of the vascular components was performed with a focus on lympho

42 EE compared with non-EE (changes in forearm vascular conductance at ACh3: -36.4%, P=0.007).

43 educed EDD in lowlanders (changes in forearm vascular conductance from sea level: ACh1: -52.7+/-19.6%

44 y anti-VEGF treatments, suggesting a retinal vascular contribution to the pathogenesis of AMD.

45 ascular dysfunction and is a risk factor for vascular contributions to cognitive impairment and demen

46 ary vascular insult in addition to secondary vascular damage due to ganglion cell damage.

47 onally considered as a separate disease from vascular dementia (VAD).

48 t dementia including Alzheimer's disease and vascular dementia, analyzing data from participants aged

49 l small vessel disease, the leading cause of vascular dementia.

50 healthy intima is thought to be populated by vascular dendritic cells (DCs) that, during hypercholest

51 immunostaining of endothelial makers, renal vascular densities were decreased accompanied by increas

52 we accounted for factors such as non-uniform vascular density and permeability that limit the applica

53 on of pericytes by PGE2 is a key process for vascular destabilization.

54 suppress VEGFA expression to support normal vascular development.

55 his is mediated by an excess of extracranial vascular disease (i.e. atherosclerosis) and/or of cerebr

56 and its transition with risks of subtypes of vascular disease across body mass index (BMI) categories

57 W83-derived OMVs induced significantly more vascular disease in a zebrafish larvae systemic infectio

58 revious stroke or transient ischemic attack, vascular disease, 65 to 74 years of age, female) score w

59 pathogenic basis of KIF11-associated retinal vascular disease, we generated a Kif11 conditional knock

60 ce of this bacterium in the circulation with vascular disease.

61 e targeted to modulate VSMC phenotype during vascular diseases.

62 level, CMH led to significant reductions in vascular disruption, leukocyte accumulation, and demyeli

63 Our simulations suggest that many common vascular dynamics may be emergent phenomena generated by

64 robic exercise prevented age- and WD-related vascular dysfunction across the lifespan, and this prote

65 c potential of targeting Sirt3 expression in vascular dysfunction and hypertension.

66 , obesity, diabetes, and prediabetes) causes vascular dysfunction and is a risk factor for vascular c

67 athetic nervous activity and hypoxia-induced vascular dysfunction has not been determined.

68 ral blood vessels, is a major contributor of vascular dysfunction in Alzheimer's disease (AD) patient

69 that reduced Sirt3 expression contributes to vascular dysfunction in hypertension, but increased Sirt

70 Interestingly, as micro-vascular dysfunction typically precedes the onset of ret

71 diate the associated pathogenesis, including vascular dysfunction, thrombosis, dysregulated inflammat

72 Vascular dysregulation may contribute to disc hemorrhage

73 In a large animal model of vascular embolization, it is shown that the BEM can be p

74 of nonhealers, were mainly expressed by the vascular endothelial cell cluster almost exclusively in

75 of early postnatal inactivation of Kif11 in vascular endothelial cells (ECs).

76 m of trigeminal ganglion sensory neurons and vascular endothelial cells (VEC) and found that neurons

77 Using primary human retinal vascular endothelial cells and an established human endo

78 vents that govern hemogenic specification of vascular endothelial cells and the generation of multili

79 gs are nitrated, (6) cytoplasmic vesicles in vascular endothelial cells known to stain for NADPH diap

80 naling via the S1P receptor 1 (S1PR1) in the vascular endothelial cells of lung and kidney.

81 ptional and spatial gradients-emanating from vascular endothelial cells outwards-in fibroblasts.

82 In vascular endothelial cells, cysteine metabolism by the c

83 he crosstalk between EphA4-Tie2 signaling in vascular endothelial cells, which is mediated through p-

84 erinflammatory milieu in the circulation and vascular endothelial damage markers within patients with

85 ogenitors, thus restricting these cells to a vascular endothelial fate.

86 Super responders had increased baseline vascular endothelial growth factor (VEGF) (880.0 pg/mL v

87 Vascular endothelial growth factor (VEGF) and semaphorin

88 submucosa (SIS) immobilized with heparin and vascular endothelial growth factor (VEGF) could be impla

89 roduction of anti-angiogenic drugs targeting vascular endothelial growth factor (VEGF) has transforme

90 nthase 2 are uniquely sensitive to increased vascular endothelial growth factor (VEGF) stimulation du

91 Anti-vascular endothelial growth factor (VEGF) treatment of n

92 OPT-302 is a novel inhibitor of vascular endothelial growth factor (VEGF)-C and VEGF-D.

93 Herein, we identified that vascular endothelial growth factor (VEGF)-C, a potent ly

94 tinopathy, is driven by chronic elevation of vascular endothelial growth factor (VEGF).

95 Vascular endothelial growth factor A (VEGF-A) and its bi

96 ntibodies targeting 2 proangiogenic factors, vascular endothelial growth factor A (VEGFA) and angiopo

97 Blockade of vascular endothelial growth factor A (VEGFA) and angiopo

98 Anti-vascular endothelial growth factor acts faster than lase

99 the potential differential efficacy of anti-vascular endothelial growth factor agents in the treatme

100 Treatment with anti-vascular endothelial growth factor agents.

101 eriodontal bone level and the expressions of vascular endothelial growth factor and core-binding fact

102 Adeno-associated virus 8-vascular endothelial growth factor C (AAV8-VEGF-C) was i

103 In the adult brain, vascular endothelial growth factor D (VEGFD) is required

104 Population: Eyes receiving intravitreal anti-vascular endothelial growth factor injections from July

105 dothelial cells (BECs) secreted higher VEGF (vascular endothelial growth factor) and lower TSP-1 (thr

106 LAN was associated with reduced hippocampal vascular endothelial growth factor-A (VEGF-A) in both ma

107 xes, specifically whether macrophage-derived vascular endothelial growth factor-A (Vegf-A) is crucial

108 Transforming growth factor-beta(1) and vascular endothelial growth factor-A secretion was measu

109 pretransfected with adeno-associated virus 1-vascular endothelial growth factor-A165 under control of

110 y reported a feedback loop between PROX1 and vascular endothelial growth factor-C (VEGF-C) signaling.

111 Modulation of vascular endothelial growth factor-mediated immune suppr

112 The role of vascular endothelial signals in tailoring the phenotype

113 During the immune response the vascular endothelium is constantly perturbed by biologic

114 his delicate coating of cells, including the vascular endothelium, regulates permeability, leukocyte

115 nonuclear cells prevents activation of human vascular endothelium, suggesting a potential role of the

116 In particular, pulmonary vascular engraftment of miR-210-positive interstitial lu

117 Use of the vascular enlargement sign in indeterminate cases was als

118 meta-analysed the risk ratio (RR) for major vascular events (a composite of cardiovascular death, my

119 median 10.0 years of follow-up, 52,251 major vascular events (MVEs), including 7,326 major coronary e

120 ring significantly reduced the risk of major vascular events (n=3519) in older patients by 26% per 1

121 core was associated with risk for both major vascular events (P(trend)=0.005) and major coronary even

122 e coronavirus disease 2019 (COVID-19), major vascular events have been reported.

123 a subset of the Randomized Trial to Prevent Vascular Events in HIV (REPRIEVE) participants.

124 There was no benefit for major vascular events in patients without multiple clinical ri

125 e probabilities of hepatocellular carcinoma, vascular events, and nonhepatic cancers were not differe

126 Treatment effects on total adjudicated vascular events, overall and by vascular territory, were

127 nteraction)=0.02; 2.7% versus 1.7% for major vascular events, P(interaction)<0.0001).

128 controlling environmental signals that guide vascular fate and assembly, thereby further informing ou

129 hibit delayed re-vascularization and reduced vascular fenestration after engraftment, partially impai

130 reasing recognition that e-cigarettes impact vascular function across multiple organ systems.

131 ism plays an important role in modulation of vascular function and BP in experimental models in vivo

132 n hypertension, but increased Sirt3 protects vascular function and decreases hypertension.

133 he current study aims to investigate retinal vascular function and its relationship with systemic ant

134 oduction and inactivation when investigating vascular function in humans ABSTRACT: Haemoglobin (Hb) m

135 ted sympathetic nervous activity and reduced vascular function in lowlanders, and Andean highlanders

136 useful indexes for noninvasive monitoring of vascular function in retinas.

137 PVAT's contributions to vascular function include more than production of vasoac

138 ur results depict the temporal impairment of vascular function over the lifespan in mice, acceleratio

139 cubated overnight with or without STBEVs and vascular function was assessed using wire myography.

140 tissue cells initiate and regulate important vascular functions in disease, especially intimal hyperp

141 hingosine 1-phosphate) signaling coordinates vascular functions in other organs, and S1P(1) (S1P rece

142 ion in TGFbeta1 signaling and termination of vascular growth.

143 on, lipids and lipoproteins, and measures of vascular health over the MT, which can increase a woman'

144 uggest that combination treatments targeting vascular health, amyloid-beta, and tau levels may more e

145 imal paternal low protein diet for offspring vascular homeostasis and define the sperm and seminal pl

146 associated with endothelial dysfunction and vascular hyperpermeability.

147 id assay to identify potential regulators of vascular identity.

148 etermine the effect of ustekinumab on aortic vascular inflammation (AVI) measured by imaging, and key

149 of interferon genes) play a critical role in vascular inflammation and destruction.

150 hibited the development of periodontitis and vascular inflammation and remarkably blocked the increas

151 indings unveil the role of a novel lncRNA in vascular inflammation by cis-regulating MAP3K4 via a p38

152 endothelial cells (ECs) is a crucial step in vascular inflammation.

153 fluences platelet plug formation at sites of vascular injury (primary hemostasis).

154 Here we show that vascular injury in rodent carotid arteries induces YY1 e

155 e their presence was aligned with regions of vascular injury.

156 contrast to POAG, which might show a primary vascular insult in addition to secondary vascular damage

157 Platelets are blood cells responsible for vascular integrity preservation.

158 ZO-1 and occludin, key mechanisms underlying vascular integrity.

159 ng a potential role of the TLR2-responses in vascular integrity.

160 rther provide a potential mechanism by which vascular interactions facilitate microglial colonization

161 There is far less known about microglia-vascular interactions, particularly under healthy steady

162 platelet therapy (DAPT) following peripheral vascular intervention (PVI), there are limited data on a

163 Here we show that obstruction of vascular invasion during bone healing favours chondrogen

164 No vascular invasion or cellular atypia were evident.

165 On explant, vascular invasion was found in 23.7% of AC-DS versus 16.

166 , (2) promotes angiogenesis, (3) facilitates vascular invasion, and (4) preserves the structural inte

167 splant, tumor diameter, tumor pathology, and vascular invasion, female sex was associated with a 25%

168 Vascular K(ATP) channel function (topical glibenclamide

169 l system, e.g. colonization of continents by vascular land plants in late Paleozoic, would certainly

170 olar-capillary barrier, triggering pulmonary vascular leak thus inducing acute lung injury (ALI).

171 n vivo efficacy in an streptozotocin-induced vascular leakage model (rat) and preliminary pharmacokin

172 We hypothesized that retinal vascular leakage would be associated with brain swelling

173 rmacological tools ameliorates inflammation, vascular leakage, neurodegeneration, and neovascularizat

174 characterized by endothelial dysfunction and vascular leakage.

175 utic opportunity for the treatment of septic vascular leakage.

176 widely heterogenous depending on tissue and vascular localization.

177 The most common type of vascular loop was type II (right: 69.14%; left: 58.75%).

178 The presence of vascular loops is not associated with most auditory symp

179 utrophils shed extracellular vesicles in the vascular lumen and that inhibition of extracellular vesi

180 In-vivo, newly recruited cells on the vascular lumen express MC markers and at later times the

181 expressed in the main population of resident vascular macrophages.

182 abnormalities, such as infection or maternal vascular malperfusion, can provide important information

183 All patients underwent a preoperative vascular mapping with Doppler ultrasound (US), and only

184 anti-VEGF treatments did not impact retinal vascular measurements (P = .324-.986).

185 show that the circulating miR-122 regulates vascular miR-204 as miR-122 inhibition decreases miR-204

186 ion appeared to be mediated by mitigation of vascular mitochondrial oxidative stress and inflammation

187 e the investigation of mechanisms underlying vascular morphogenesis.

188 types, including astrocytes, microglia, and vascular mural cells (VMCs).

189 indings were classified by the study team as vascular, neoplastic, congenital, other neurologic, or n

190 that this network is separate from the blood vascular network and that it drains interstitial fluid f

191 In this study we exploited the hyaloid vascular network in murine eyes, which naturally undergo

192 h using a one-dimensional model of the human vascular network.

193 rificial templates for patterning perfusable vascular networks in engineered tissues have been constr

194 Telestroke provides access to vascular neurology expertise for hospitals lacking strok

195 argeting pericytes and endothelial cells for vascular normalization, are proving to effectively deliv

196 oma, episcleritis and scleritis, and retinal vascular occlusion in patients with SLE deserves vigilan

197 blood probing during the hyperacute stage of vascular occlusion is crucial to assess the role of infl

198 Acute retinal vascular occlusions are common causes of visual impairme

199 The ability of MC(TC)s to affect vascular organization during fetal lung development was

200 ipapillary and macular retina and changes in vascular parameters have been identified.

201 tissue inflammation and is prominent in most vascular pathological conditions such as atherosclerosis

202 Sirolimus plus nintedanib prevented vascular pathology in the oral mucosa, lungs, and liver

203 Collectively, the evidence suggests that vascular pathology is a likely pathogenic contributor to

204 al similarities in clinical presentation and vascular pathology.

205 support diagnosis of MS induced cardiac and vascular pathophysiology, to assess prognosis, and under

206 sm underlies an interplay between microglia, vascular patterning and tissue mechanics within the CNS.

207 The presence of the vascular pedicle further enhanced bone formation.

208 antified 11 candidate miRNAs associated with vascular performance and shuttled by CD31(+) EVs in a la

209 normalized, the retinal and choriocapillaris vascular perfusion showed focal defects in every layer.

210 ation after engraftment, partially impairing vascular permeability and glucose delivery to beta-cells

211 tical illnesses is associated with increased vascular permeability and mortality.

212 Vascular permeability and plasma leakage are immune-path

213 ated acute pulmonary damage through reducing vascular permeability changes and recruitment of neutrop

214 ss is known about downstream mechanisms (ie, vascular permeability controlled by endothelial cells [E

215 ted by immunostaining with isolectin B4, and vascular permeability was analyzed by fluorescein angiog

216 angiotensin II to control vasodilatation and vascular permeability.

217 athophysiology of U-HAE increasing the basal vascular permeability.

218 complicate interpretations in the context of vascular physiology and pathophysiology.

219 chine learning approaches to a comprehensive vascular plant database for the United States and genera

220 teracts with two rice transcription factors, VASCULAR PLANT ONE-ZINC FINGER 1 (OsVOZ1) and OsVOZ2, an

221 uisite for high photosynthetic capacities in vascular plants and a key driver of the abrupt Cretaceou

222 earity between the two bryophyte genomes and vascular plants is limited, suggesting extensive rearran

223 the regulation of water and carbon fluxes in vascular plants, finally examining specific evidence for

224 found mainly in the secondary cell walls of vascular plants, where it contributes to mechanical stre

225 by high abundance of retroelements unlike in vascular plants.

226 activate photoprotection, as is the case in vascular plants.

227 pha, that is homologous to MIXTA proteins in vascular plants.

228 and demonstrate that a window of heightened vascular plasticity is coupled to the reestablishment of

229 These cells formed a perineural vascular plexus from which angiogenic sprouts originated

230 ows less involvement of superficial and deep vascular plexus in NAION in contrast to POAG, which migh

231 merular size and is present primarily on the vascular pole size.

232 were measured on all glomeruli containing a vascular pole.

233 actively represses muscle differentiation in vascular progenitors, thus restricting these cells to a

234 is critical for brain health, and endogenous vascular protective pathways may provide therapeutic tar

235 ion and signaling, we demonstrate a critical vascular protective role for endothelial S1P(1) in the m

236 in kidney and pancreas transplantation when vascular reconstruction is needed and additional vessels

237 dings reveal the spatiotemporal evolution of vascular remodeling after stroke and demonstrate that a

238 the cell behaviors underlying each stage of vascular remodeling and identify a pathway required for

239 surrounding the infarct, but whether and how vascular remodeling contributes to recovery are unclear.

240 time-course of the development of pulmonary vascular remodeling in PAH rats.

241 is a fatal disease characterized by profound vascular remodeling in which pulmonary arteries narrow b

242 iogenic apelin as a key mediator of coronary vascular repair and a pharmacotherapeutic target for imm

243 al angiogenesis, suggesting a dual effect on vascular repair upon FECH inhibition, without ocular tox

244 p = 0.005) and tended to decrease pulmonary vascular resistance (-83 +/- 33 dynes; p = 0.07).

245 Additionally, pulmonary vascular resistance (PVR) 2.2 to 3.0 WU, considered prev

246 mal lesions, resulting in elevated pulmonary vascular resistance and right heart failure.

247 As compared to pulmonary vascular resistance at rest, slope of increase in pulmon

248 ients with HFrEF leads to increased systemic vascular resistance, which constrains stroke volume, car

249 vascular coupling systematically affects the vascular response in small retinal vessels in order to m

250 ide a connection to the ECM that facilitates vascular responsiveness contributing to blood pressure r

251 oportion of Chinese adults, with the highest vascular risk among those remained MUOO.

252 s were independent of socio-demographics and vascular risk factors (body mass index, smoking, diabete

253 Demographic and vascular risk factors and levels of outdoor pollutants w

254 heric strokes particularly when conventional vascular risk factors are not present.

255 ke, particularly in younger patients without vascular risk factors.

256 ancy- and puberty-associated accentuation of vascular risk, also seen in vEDS patients, was rescued b

257 Mice lacking Klf5 in VSMCs exacerbate vascular senescence and progression of angiotensin II (A

258 y tone and tissue perfusion but the involved vascular-sensing mechanisms and disease consequences rem

259 ogether, our data show that GPRC5B regulates vascular SMC tone and differentiation by negatively regu

260 These vascular SMCs, termed degradative SMCs, compromise the m

261 the link between mitochondrial dynamics and vascular smooth muscle cell (VSMC) senescence.

262 ediated cholesterol depletion remodels total vascular smooth muscle cell cytoskeletal orientation tha

263 he human gene encoding NOTCH3 and results in vascular smooth muscle cell degeneration, stroke, and de

264 , E-selectin, MCP-1) in endothelial cells or vascular smooth muscle cells and decreased monocytes adh

265 at has aggregated within the mitochondria of vascular smooth muscle cells can drive an hour-long disr

266 n vascular cells, like endothelial cells and vascular smooth muscle cells, cardiac myocytes and infla

267 ng into nonmyocyte cardiac lineages, such as vascular smooth muscle cells, pericytes, and fibroblasts

268 imal hyperplasia, diseases linked to loss of vascular smooth muscle differentiation.

269 the importance of smooth muscle response to vascular stress and phenotypic modulation of this cell t

270 graphy (FA) is a procedure used to image the vascular structure of the retina and requires the insert

271 Existing methods to reconstruct vascular structures from a computerized tomography (CT)

272 ents referred to the population-based Oxford Vascular Study (2011-2020) with suspected TIA/minor stro

273 In a population-based study (Oxford Vascular Study/2002-2018) of patients with a first ICH w

274 Patterns for vascular surgery outcomes resembled general surgery; how

275 y, and 52,025 pairs of patients admitted for vascular surgery.

276 mb, without changing heart rate (P = 0.6) or vascular-sympathetic baroreflex gain (P = 0.85).

277 play an important role in maintenance of the vascular system and the repair after injury.

278 and complete responders, where parts of the vascular system are occluded for the first and the whole

279 ction with the evolution of a more efficient vascular system for the transport of water, composed of

280 sac and the eye choriocapillaris and hyaloid vascular systems, develops at least in part via hemovasc

281 Using RSOM to examine the responses to vascular-targeted photodynamic therapy in mice with subc

282 er preclinical disease models (e.g. stroke), vascular-targeted therapeutics, and hemodynamic data fro

283 adjudicated vascular events, overall and by vascular territory, were summarized by marginal proporti

284 A prevailing dogma is that inhibition of vascular thrombosis by antagonizing platelet integrin al

285 ere similar in the incidence of reoperation, vascular thrombosis, posttransplant lymphoproliferative

286 ezo1 mechanosensitive ion channel in guiding vascular tip cells in pathfinding.

287 sheaths, pollen grains, and surrounding the vascular tissues of anthers, suggesting that OsNLA1 is i

288 olemman phosphorylation in the regulation of vascular tone and BP and suggest a novel mechanism, and

289 human cardiovascular physiology, regulating vascular tone and smooth-muscle cell phenotype.

290 that phospholemman phosphorylation regulates vascular tone in vitro and that this mechanism plays an

291 smembrane calcium channels that can regulate vascular tone, in modulating AAA formation.

292 Kaposi's sarcoma (KS) is a rare vascular tumor associated with human herpesvirus (HHV)-8

293 ularly in peripheral territories examined by vascular ultrasound.

294 artery calcification score and 2-dimensional vascular ultrasound.

295 sis as assessed by bilateral carotid/femoral vascular ultrasound.

296 re discovered between the single- and triple-vascular-vessel lesion groups.

297 a hypoxia-response element markedly promotes vascular volume and blood flow, increased proliferation

298 uned from histology data, including relative vascular volume, mean vessel diameter, and distance from

299 a novel way to regulate brain entry through vascular wall remodeling.

300 Cells in vascular walls are exposed to blood pressure variability