ライフサイエンスコーパス: arteriole

1 al response to hyperglycemia at the efferent arteriole.

2 supplied by a centrally placed thick-walled arteriole.

3 d in the absence of physical contact with an arteriole.

4 travascular pressure in the upstream feeding arteriole.

5 ng of intramural small coronary arteries and arterioles.

6 stress secondary to metabolic dilatation of arterioles.

7 versus CKD5 arterioles and in CKD5 versus PD arterioles.

8 unologic, and stress-response cascades in PD arterioles.

9 gene that is strongly induced in developing arterioles.

10 ion declines with age in coronary resistance arterioles.

11 chanism is embolization and occlusion of end arterioles.

12 marily from venules, and the CBV signal from arterioles.

13 h wider retinal venules and narrower retinal arterioles.

14 ontributes to functional dilatation in these arterioles.

15 the vascular smooth muscle layer of terminal arterioles.

16 alter the proper functioning of the adjacent arterioles.

17 phrine activation of alpha1ARs on peripheral arterioles.

18 lar remodeling in the precapillary pulmonary arterioles.

19 the glomeruli, peritubular capillaries, and arterioles.

20 ar BAPTA causes vasoconstriction in adjacent arterioles.

21 nitrate (0.013-4.4 nmol/min) over resistance arterioles.

22 perivascular endfeet surrounding parenchymal arterioles.

23 ivascular regions of both large arteries and arterioles.

24 pid-induced endothelial dysfunction in human arterioles.

25 pitated with LOX-1 and CD32 from CRP-treated arterioles.

26 logy, which showed evidence of remodeling of arterioles.

27 z vasomotor oscillation in diameter of local arterioles.

28 s in penetrating arterioles, but not in pial arterioles.

29 ) mice, which was present up to the afferent arterioles.

30 of vesicle-mediated transport in penetrating arterioles.

31 ed by intravital microscopy of laser-injured arterioles.

32 olume (CBV)-fMRI from individual venules and arterioles.

33 scored as negative (0), small deposits in 1 arteriole (1+), small/large deposits in >1 arterioles (2

34 1 arteriole (1+), small/large deposits in >1 arterioles (2+), or at least extensive deposits in most

35 mum); smoking also was associated with wider arterioles (2.1 mum; 95% CI, 1.3-2.9 mum).

36 (2+), or at least extensive deposits in most arterioles (3+).

37 Thinner arterioles (-3.2 mum; 95% confidence interval [CI] -4.4

38 venules (median RBC velocity in first-order arterioles, 5 minutes after administration was zero for

39 re/shell architecture previously observed in arterioles also occurs in venules, (2) plasma leakage pe

40 olated vascular smooth muscle cells from CAD arterioles, although mRNA or total cellular protein expr

41 tion alone is not sufficient to dilate these arterioles; an additional EC calcium-dependent signallin

42 er at the transition between the penetrating arteriole and first order capillary, linking blood flow

43 travascular pressure in the upstream feeding arteriole and promoting its rupture at the site of SMC l

44 Mean arteriole and venule diameter in the inner and outer zon

45 In all, 279 802 arterioles and 285 791 venules from 5947 participants (m

46 ion of coronary, skeletal muscle and adipose arterioles and a sustained increase in systemic blood pr

47 (-/-) mice demonstrated a marked decrease in arterioles and an increase in the number and volume of v

48 increases in total eNOS content in terminal arterioles and capillaries (P < 0.001) in the three cond

49 ecreased significantly following training in arterioles and capillaries (P < 0.001).

50 d eNOS ser(1177) phosphorylation in terminal arterioles and capillaries (P < 0.05), but the latter ef

51 sseminated platelet-rich thrombi in terminal arterioles and capillaries of major organ tissues in the

52 oretinal vasculature a novel segment between arterioles and capillaries, herein called the transition

53 rease their energy supply by dilating nearby arterioles and capillaries.

54 ex vivo on human subcutaneous adipose tissue arterioles and endothelial cells.

55 hese findings across models (cells, isolated arterioles and humans) support the hypothesis that eleva

56 ntial gene expression in control versus CKD5 arterioles and in CKD5 versus PD arterioles.

57 in the endothelium of muscularized pulmonary arterioles and in cultured pulmonary ECs from iPAH, cont

58 irments in the myogenic response of afferent arterioles and in renal blood flow autoregulation, which

59 ro in endothelial cells, ex vivo in isolated arterioles and in vivo in humans.

60 eling leads to narrowing of distal pulmonary arterioles and increased pulmonary vascular resistance.

61 in the walls of leptomeningeal and cortical arterioles and is likely a contributory factor to vascul

62 to a reduced vasodilatation of intracerebral arterioles and is reversible by reducing tau production.

63 o ferric chloride (FeCl3)-injured mesenteric arterioles and laser-induced injury of cremaster muscle

64 ed activation of metabolic processes in CKD5 arterioles and of inflammatory, immunologic, and stress-

65 r processes along capillaries, pre-capillary arterioles and post-capillary venules.

66 cting both cerebral cortical capillaries and arterioles and resulting from Abeta deposition within th

67 or novel modes of activation of the AT1 R in arterioles and suggest that mechanically activated AT1 R

68 cts myogenic constriction in skeletal muscle arterioles and to determine underlying cellular mechanis

69 cts, lobules, microcysts, blood vessels, and arterioles and to identify invasive tumor through distin

70 as rapidly and completely stopped in all the arterioles and venules (median RBC velocity in first-ord

71 Episodic flow within the SVP arterioles and venules and poor visualization of flow in

72 segment is determined by the distribution of arterioles and venules and their respective relative flo

73 id artery, the jugular vein, and cremasteric arterioles and venules in Apoe(-/-)and CatG-deficient mi

74 Less tortuous retinal arterioles and venules were associated with all glaucoma

75 and wall shear stress (WSS) were measured in arterioles and venules, and compared between DR and C su

76 with specificity at the level of individual arterioles and venules.

77 ladder capillaries which connect peripheral arterioles and venules.

78 ignificant increases in velocity and flow in arterioles and venules.

79 perfused vascular tree, including arteries, arterioles and venules.

80 Narrower retinal arterioles and wider retinal venules conferred long-term

81 Narrower retinal arterioles and wider retinal venules have been associate

82 n hearts, this causes a loss of arteries and arterioles and, despite a high capillary density, dimini

83 l model of the sympathetic innervation of an arteriole, and used it to test the hypothesis that respi

84 lial endfeet contacting capillaries, but not arterioles, and that capillary dilations often follow sp

85 Here we show that parenchymal arterioles are responsible for 50% of the extracted O2 a

86 capillaries (37%), while for deeper regions arterioles are responsible for 61% of the total pressure

87 rted by local and spreading responses in the arterioles associated with those fibres.

88 ixed values, while the particles leaving the arteriole at the outlet are removed from the system.

89 expression of apoE4, but not apoE3, reduced arteriole blood flow, impaired spatial learning, and inc

90 Ca(2+) signaling regulates capillary but not arteriole blood flow.

91 channels in control tumors but a network of arterioles, bona fide capillaries, and venules in FGF9-e

92 e, and inhibited transcytosis in penetrating arterioles, but not in pial arterioles.

93 sponsiveness to TNF-alpha in KRIT1 deficient arterioles, but not venules.

94 um), more selective P2X antagonists, dilated arterioles by 41.0 +/- 5.3% and 55.2 +/- 6.1% respective

95 It dilates arterioles by activating large-conductance Ca(2+)-activa

96 Thrombosis was induced in cortical arterioles by laser irritation.

97 of TGF-beta Furthermore, in the PD parietal arterioles, C1q and terminal complement complex abundanc

98 The results show that, independent of arterioles, capillaries actively dilate and regulate blo

99 aces include a variety of passageways around arterioles, capillaries and venules in the brain, along

100 cking the normal hierarchical arrangement of arterioles, capillaries and venules.

101 city, vessel diameter, and therefore flow in arterioles, capillaries, and venules in all nine subject

102 Rs was greater in upstream feed arteries and arterioles compared to downstream arterioles, with alpha

103 tory dilation observed in the normal retina, arterioles constrict in response to an oxygen deficiency

104 mal arteriole vascular tone, which result in arteriole constriction and dilation, respectively, alter

105 Capillary, but not arteriole, constriction also occurred in vivo in a mouse

106 measured as the average diameter of retinal arterioles (CRAE) and venules (CRVE), and summarized as

107 ion of white matter hyperintensities via end-arteriole damage may protect against secondary brain atr

108 ath-applied VP significantly constricted SON arterioles (Delta-41 +/- 7%) via activation of the V1a r

109 , infarct size, apoptosis, both vascular and arteriole density, and cell proliferation at week 4 afte

110 w recovery involves an increase in capillary/arteriole density, endothelial nitric oxide synthase/Akt

111 lowed by improved blood perfusion, capillary/arteriole density, skeletal muscle architecture, and cel

112 In contrast, dilation of arterioles depends on NMDA receptor activation and Ca(2+

113 that acute COX-1 inhibition reduces resting arteriole diameter but fails to affect vasodilation in r

114 e responsible for the long-lasting change in arteriole diameter caused by theta burst neural activity

115 Fourth, fluctuations in arteriole diameter coherently drive fluctuations in bloo

116 creases in cerebral blood volume ([HbT]) and arteriole diameter relative to the awake state, two to f

117 ntrinsic ultra-slow (0.1 Hz) fluctuations in arteriole diameter, provides this link.

118 responsible for regulating capillary but not arteriole diameter.

119 neurons and astrocytes that signal to alter arteriole diameter.

120 First, they closely track changes in arteriole diameter.

121 ) and that the effect has an impact on basal arteriole diameter.SIGNIFICANCE STATEMENT The field of a

122 with FITC conjugated BSI-lectin labeling and arteriole diameters were compared before and five minute

123 d, flow/pressure decreases evoke parenchymal arteriole dilation and increased resting pyramidal neuro

124 This hypothesis has been challenged, as arteriole dilation can occur in the absence of glial Ca(

125 is reduced, light-evoked capillary, but not arteriole, dilation is abolished.

126 ibute to metabolic dilatation as they dilate arterioles directly upstream in response to vasoactive a

127 Arterioles displayed a vasoconstriction response to KCl

128 into the smooth muscle surrounding cerebral arterioles, driving vasodilation.

129 from residual vasomotor activity as well as arteriole dynamics driven by self-generated movements an

130 reatment midway between a FA and its primary arteriole eliminated ROV in the FA along with conducted

131 o endothelium midway between FAs and primary arterioles eliminated ROV only in FAs.

132 ply growth factors to preexisting collateral arterioles enabling them to grow.

133 07, was also associated with central retinal arteriole equivalent (P=6.5x10(-12)).

134 hich is also associated with central retinal arteriole equivalent.

135 al venule equivalent and the central retinal arteriole equivalent.

136 in arterial smooth muscle cells, constricted arterioles ex vivo and in vivo and increased systemic bl

137 ogenic responsiveness of renal preglomerular arterioles ex vivo and promoted cellular contraction in

138 or lipid-induced endothelial dysfunction in arterioles ex vivo.

139 e contractile proteins, whereas the upstream arteriole exhibited a loss of SMCs.

140 PD arterioles exhibited particular upregulation of the comp

141 Endfeet with eHACSs were present only around arterioles exhibiting inversion of NVC.

142 Similarly, isolated arterioles exposed to 1 h of intraluminal shear stress (

143 III1H,8-10 and FNIII1H applied to EC-denuded arterioles failed to produce any dilatation indicating t

144 The reduction of flow velocity in cortical arterioles following thrombosis was significantly attenu

145 dent vasodilatation was impaired in coronary arterioles from aged rats (maximal relaxation to bradyki

146 In arterioles from CAD subjects, H2O2-induced dilation was

147 induces arteriolargenesis - the formation of arterioles from capillaries - in a model of physiologica

148 dothelial dysfunction, whereas in resistance arterioles from glycolytic muscle, alterations in both n

149 Internal diameter changes of resistance arterioles from human adipose and atrial tissue were mea

150 elevance of Sirt3 depletion was confirmed in arterioles from human mediastinal fat in patients with e

151 dings were validated in omental and parietal arterioles from independent pediatric control (n=5), CKD

152 hibited alpha-adrenergic vasoconstriction in arterioles from mice and hypertensive humans, an effect

153 After exposure to BIBR-1532, arterioles from non-CAD subjects maintained the magnitud

154 with advancing age are heterogeneous between arterioles from oxidative and glycolytic muscles.

155 In resistance arterioles from oxidative muscle, loss of nitric oxide s

156 signalling contribute to the dysfunction in arterioles from oxidative muscles as compared with those

157 ctional adaptations that occur in resistance arterioles from oxidative muscles differ from those that

158 Remodeled pulmonary arterioles from SU-5416/hypoxia-PAH rats and monocrotali

159 a physiological mechanism of vasodilation in arterioles from subjects with CAD.

160 hibitor) abolished flow-mediated dilation in arterioles from subjects without CAD, whereas polyethyle

161 (2) isolated and pressurized skeletal muscle arterioles from swine, and (3) humans.

162 We microdissected omental arterioles from tissue layers not directly exposed to PD

163 Mesenteric arterioles from wild type (WT) and SMTNL1 global knock-o

164 nd a panniculitis with sparse, subtle, intra-arteriole, gray amorphous deposits that, on analysis by

165 In human arterioles, H2O2-induced dilation is impaired in CAD, wh

166 Neighbouring penetrating arterioles had different orientation preferences.

167 that functional vasodilatation in resistance arterioles has an endothelial cell (EC)-dependent compon

168 s to the disease site i.e., distal pulmonary arterioles has been one of the major challenges in achie

169 contrast, most in vivo studies of downstream arterioles have disproved these hypotheses and instead h

170 udies testing these hypotheses in downstream arterioles have failed to find evidence of intrinsic O2

171 nt where a large number of the pre-capillary arterioles have low perfusion, low haematocrit, and are

172 on has been reported in most skeletal muscle arterioles; however, unique alterations in signalling co

173 1.20 per 1-SD increase) and narrower retinal arterioles (HR, 1.06; 95% CI, 1.01-1.11; HR, 1.14; 95% C

174 gradation impacted dilation of a penetrating arteriole in cortex.

175 Venous segments were deviated toward the arterioles in 6 of the 7 cases.

176 pacities were applied directly to resistance arterioles in cremaster muscles of anaesthetized (pentob

177 Yet the diameters of arterioles in distant (>5 mm), mirrored transhemispheric

178 vasoreactivity was absent in control tumors, arterioles in FGF9-expressing tumors could constrict and

179 The flow velocity of cortical arterioles in mice was measured in vivo under 2-photon l

180 ells causes the marked tortuosity of retinal arterioles in MSMDS.

181 ere, we show in mice that CO(2)/H(+) dilates arterioles in other chemoreceptor regions, thus demonstr

182 as well as surface arteries and penetrating arterioles in rat visual cortex (where orientation maps

183 eptors, particularly on endothelial cells of arterioles in the brain and immune cells, which is in li

184 Arterioles in the cutaneous microcirculation frequently

185 al activity and communicating it to upstream arterioles in the form of an electrical vasodilatory sig

186 zation of TRPV1 to smooth muscle of terminal arterioles in the heart, adipose tissue and skeletal mus

187 Arterioles in the peripheral microcirculation are exquis

188 is, or the lumenal expansion of pre-existing arterioles in the presence of an upstream occlusion, is

189 collateral arteries and increased numbers of arterioles in the thigh.

190 ffects on CO(2)-induced dilation of cerebral arterioles in vivo.

191 Vesicle-mediated transfer of albumin in arterioles increased 3 to 10-fold in Apom(-/-) mice, whe

192 ncreases in flow/pressure within parenchymal arterioles increased the firing activity of a subtype of

193 Flow/pressure increases within parenchymal arterioles increased vascular tone and simultaneously de

194 om both neurons and astrocytes, which dilate arterioles, increasing in turn cerebral blood flow (CBF)

195 Isolated rat and human arterioles incubated with adenosine (10 nmol/L) or ADK i

196 ed greater volume, with evidence of tortuous arterioles indicative of arteriogenesis (n=6-8 per group

197 ontraction while observing feed arteries and arterioles initiated ROV, which increased with contracti

198 elet accumulation in laser-induced cremaster arteriole injury, and PDI(ss-oo) mice had attenuated pla

199 The field of astrocyte-neuron and astrocyte-arteriole interactions is currently in a state of refine

200 Upon release from arterioles into the red pulp sinuses, T cells latched on

201 cise, vasodilatation ascends from downstream arterioles into upstream feed arteries (FAs).

202 , functioning at the mercy of their upstream arterioles, into independent contractile units that were

203 branches to travel from afferent to efferent arterioles) is relatively independent of glomerular size

204 tment with gAd improved insulin responses in arterioles isolated from HFD rats, which was blocked by

205 ally, conducted vasodilation was measured in arterioles isolated from the right atrial appendages of

206 r insulin-induced vasodilatation compared to arterioles kept under no-flow conditions.

207 ast with LacZ-positive cells in the afferent arterioles, LacZ-positive cells in the glomerular tuft d

208 tion and structural remodelling of pulmonary arterioles, leading to chronic elevation of pulmonary ar

209 This renders arterioles less responsive to K(+) released from astrocy

210 ate cerebral blood flow at the capillary and arteriole levels.

211 Our previous work showed that cortical arteriole lumen diameter is regulated by N-methyl-d-aspa

212 phages, accompanied by enhanced formation of arterioles, may be responsible for shift of Hmox1(-/-) m

213 o measure densitometry differences (adjacent arterioles minus DH [DeltaA] or venules minus DH [DeltaV

214 plus spironolactone in vivo, which decreased arteriole muscularization and pulmonary hypertension in

215 ease in pulmonary artery pressure and distal arteriole muscularization.

216 isc margin) were summarized as mean width of arterioles (MWa) and mean width of venules (MWv).

217 s with patchy necrosis and fibrin thrombi in arterioles (n = 2).

218 labeling of renin cells along renal afferent arterioles of adult mice.

219 c 3D simulations to study plasma skimming in arterioles of diameters 20 to 32 microns.

220 in the endothelial layer of capillaries and arterioles of human skeletal muscle.

221 sopressin-mediated vascular responses in SON arterioles of hypothalamic brain slices of Wistar or VP-

222 erstitial cells, in the remodelled pulmonary arterioles of rats, cows and humans susceptible to hypox

223 mote platelet-neutrophil aggregation in lung arterioles of SCD mice in vivo and SCD human blood in mi

224 nd restored microvascular blood flow in lung arterioles of SCD mice in vivo and SCD human blood in mi

225 The extent to which smooth muscle-covered arterioles or pericyte-covered capillaries control vasom

226 No reperfusion of arterioles or venules was observed at M3 on FA or SS-WF

227 vessels and minute flows down to 0.3 mm/s in arterioles or venules were readily detectable at depths

228 order typified by occlusion of the pulmonary arterioles owing to endothelial dysfunction and uncontro

229 Training decreased NOX2 content (arterioles P < 0.001; capillaries P < 0.001), but there

230 nuated retinal vascular pulsation amplitude (arterioles P = .028; venules P < .0001).

231 ut there was no change in p47(phox) content (arterioles P = 0.101; capillaries P = 0.345).

232 no change in eNOS ser(1177) phosphorylation (arterioles P = 0.802; capillaries P = 0.311), but eNOS s

233 contribute to the regulation of parenchymal arteriole (PA) tone in response to hemodynamic stimuli (

234 assessed using ultrasound, and capillary and arteriole parameters were assessed using immunohistochem

235 th muscle cells of the afferent and efferent arterioles, parietal epithelial cells, and three types o

236 Remodeling of distal pulmonary arterioles (PAs) associated with marked accumulation of

237 Here, using parenchymal arterioles (PAs) from within the brain, we determined th

238 PD fluid and used adjacent sections of four arterioles per patient for transcriptomic and proteomic

239 ressed increased StAR in remodeled pulmonary arterioles, providing a basis for investigating hypoxia-

240 val in vitro Optimal inhibition of pulmonary arteriole Raptor was achieved by treatment with Staramin

241 Renal preglomerular arterioles regulate vascular tone to ensure a large pres

242 TGF-induced vasoconstriction of the afferent arteriole results from the enhanced effect of several va

243 Microarray analysis of mutant arterioles revealed upregulation of genes usually expres

244 onsistently illustrated as one-way flow from arteriole(s) to venule(s) with no integration of the cap

245 sis by fabricating and perfusing multi-layer arteriole-scale human tissue-engineered blood vessels (T

246 dimensional model of HGPS that replicates an arteriole-scale tissue engineered blood vessel (TEBV) us

247 Decidual spiral arteriole (SpA) remodeling is essential to ensure optima

248 s the average pulsation amplitude of retinal arterioles (SRAP) and venules (SRVP).

249 giography showed extreme corkscrew course of arterioles suggesting vessel elongation.

250 and robust dilations of upstream parenchymal arterioles, suggesting a key role of cECs in NVC.

251 Of 28 lesions analyzed, the arteriole supplying the affected area was a single side

252 zed by increased blood pressure in the small arterioles supplying blood to lungs for oxygenation.

253 xpression in the smooth muscle of resistance arterioles supplying skeletal muscle, heart and adipose

254 ascular plexus were traced to identify small arterioles supplying the affected areas.

255 ed arteries, first-, second- and third-order arterioles supplying the GM using intravital microscopy.

256 ed resistance arteries and large first-order arterioles support the hypotheses that O2 -dependent inh

257 d resistance arteries and large, first-order arterioles support the hypothesis that these vessels are

258 The luminal diameter of a common terminal arteriole (TA) controls blood flow through up to 20 capi

259 retinal macroaneurysms and adjacent retinal arterioles than to blood from retinal vein occlusions or

260 ements more similar in magnitude to adjacent arterioles than venules, supporting an arterial origin f

261 FAs reflects hyperpolarization of downstream arterioles that conducts along the endothelium into prox

262 unced reduction of flow velocity in cortical arterioles that persisted for >=90 min.

263 dy rat isolated first-order cremaster muscle arterioles the AT1 R inhibitor candesartan (10(-7) -10(-

264 al muscle microcirculation, or adipomuscular arterioles, the removal of which abolished IMVR.

265 hypertension (PAH), correlate with pulmonary arteriole thickening, which suggests that mTORC1 regulat

266 compared with the control group, whereas the arteriole to venule ratio and vascular tortuosity were s

267 central retinal vein equivalent (CRVE), the arteriole to venule ratio, tortuosity, and fractal dimen

268 he relative contributions of capillaries and arterioles to blood flow regulation remain unclear, eluc

269 hyperpolarizing signal that dilates upstream arterioles to rapidly increase local blood flow.

270 ganized, including venules, capillaries, and arterioles, to supply all of the cells with sufficient n

271 n the retrotrapezoid nucleus (RTN) maintains arteriole tone during high CO2/H(+) and disruption of th

272 On the other hand, decreasing parenchymal arteriole tone increased resting cortical pyramidal neur

273 e, we demonstrate that increased parenchymal arteriole tone significantly increased intracellular cal

274 ytes can control basal synaptic strength and arteriole tone via their resting Ca(2+) activity.

275 ot Ca(2+) was coincident with an increase in arteriole tone, and both the Ca(2+) drop and the tone ch

276 hat, in response to increases in parenchymal arteriole tone, astrocyte intracellular Ca(2+) increased

277 During increases in parenchymal arteriole tone, the pyramidal neuron response was unaffe

278 cyte Ca(2+) and that this phenomenon changed arteriole tone.

279 ascular resistance, which largely depends on arteriole tone.

280 , smooth muscle cells (SMCs) along the renal arterioles transform into renin cells until homeostasis

281 d non-dividing (Ki-67(-)), were distant from arterioles, transition zone vessels, and bone surfaces.

282 did not alter the flow velocity of cortical arterioles under physiologic conditions.

283 ed vasodilatation of the FA initiated on the arteriole using ACh microiontophoresis.

284 ulation despite robust dilations of adjacent arterioles using cyto-GCaMP3 and Lck-GCaMP6s, the most s

285 that astrocytes provide tonic regulation of arterioles using resting intracellular Ca(2+) in a manne

286 In arterioles, V, WSR, and WSS were lower in NDR (P </= 0.0

287 evoked increases or decreases in parenchymal arteriole vascular tone, which result in arteriole const

288 Inorganic nitrite dilates small resistance arterioles via hypoxia-facilitated reduction to vasodila

289 ow by providing steady-state vasodilation to arterioles via resting astrocyte Ca(2+) and the continuo

290 and laser-induced injury of cremaster muscle arterioles, we herein show that thrombi formed in Cc2(-/

291 Narrower arterioles were associated with age (0.8 mum; 95% CI, 0.

292 flow and vasodilatory responses of coronary arterioles were evaluated in all groups at the end of tr

293 Human coronary and adipose arterioles were isolated for videomicroscopy.

294 st- (1A), second- (2A) and third- (3A) order arterioles were studied in response to single tetanic co

295 e leaflets and remodeled intramural coronary arterioles, which involve tissue types that do not expre

296 -independent vasodilation in non-CAD adipose arterioles, which was reduced by paxilline, a large-cond

297 -independent vasodilation in non-CAD adipose arterioles, which was reduced by paxilline, a large-cond

298 teries and arterioles compared to downstream arterioles, with alpha2 ARs more effective than alpha1 A

299 co-fluctuations in the diameter of pairs of arterioles within the same hemisphere diminish to chance

300 eling of a venous segment close to a retinal arteriole without arteriovenous overlap were imaged by a