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1  in the radial artery, suggesting that it is endothelium-dependent.
2 nduced vasodilation in mesenteric vessels is endothelium-dependent.
3                    To test this, we measured endothelium-dependent (acetylcholine) and -independent v
4  serotonin; both P = .03); relaxation to the endothelium-dependent agonist acetylcholine was attenuat
5  Under baseline conditions, responses to the endothelium-dependent agonist acetylcholine were not aff
6 d intradermal microdialysis perfusion of the endothelium-dependent agonist acetylcholine, alone and i
7  contraction amplifies vasodilatation to the endothelium-dependent agonist ACh, whereas there was no
8              Deletion of PTP1B improved both endothelium dependent and independent NO-mediated dilati
9 tionally, obese mice demonstrate an impaired endothelium dependent and independent vasodilation to ac
10                                              Endothelium-dependent and -independent arterial vasodila
11     Intravital microscopy was used to assess endothelium-dependent and -independent arteriolar vasodi
12                          Resveratrol elicits endothelium-dependent and -independent dilation of retin
13                                              Endothelium-dependent and -independent flow-mediated vas
14 ears that the dilatation is mediated by both endothelium-dependent and -independent signalling pathwa
15 and SV graft vasomotor and flow responses to endothelium-dependent and -independent stimuli 5 years a
16 e, distal segments failed to respond to both endothelium-dependent and -independent stimuli.
17 al coronary segments that fail to respond to endothelium-dependent and -independent stimuli.
18 hy, higher white blood cell count, and lower endothelium-dependent and -independent vasodilation in t
19 ignificantly improved vascular reactivity to endothelium-dependent and -independent vasodilators as w
20  peroxynitrite (ONOO(-)) inhibitors improved endothelium-dependent and EDHF-mediated relaxations and
21                                      Forearm endothelium-dependent and endothelium-independent vasodi
22 gen species, endothelial cell apoptosis, and endothelium-dependent and endothelium-independent vasore
23                                              Endothelium-dependent and independent vasodilation was t
24 moglobin (Hb) may impact the transduction of endothelium-dependent and nitric oxide (NO)-mediated vas
25         Nebivolol but not metoprolol induced endothelium-dependent and nitric oxide-dependent relaxat
26                               Flow-mediated, endothelium-dependent and nitroglycerin-induced, endothe
27               The activation of PAR-1 causes endothelium-dependent arterial vasodilation and the rele
28   The vasorelaxation properties seemed to be endothelium dependent, as well as nitric oxide (NO) and
29 al agents (either endothelium-independent or endothelium-dependent) at 1 year.
30 y during transfusion, followed by testing of endothelium-dependent blood flow with increasing doses o
31 erol supplementation significantly increased endothelium-dependent brachial artery flow-mediated dila
32            The primary outcome was change in endothelium-dependent brachial artery flow-mediated dila
33 of isolated arteries with palmitate impaired endothelium-dependent but not vascular smooth muscle fun
34 vasodilator responses to acetylcholine (ACh; endothelium dependent) but not sodium nitroprusside (SNP
35 stal segments: incremental atrial pacing for endothelium-dependent cases; and intracoronary nitroglyc
36 kidney function and hemodynamic responses to endothelium-dependent challenge were assessed in pigs af
37 en evaluated for suspected ischemia, and the endothelium-dependent component is linked with adverse o
38 d releases endothelin-1 (ET-1) and initiates endothelium-dependent constriction.
39 lial stimulation, and initiate ET-1-mediated endothelium-dependent constriction.
40                       Thrombin did not cause endothelium-dependent contraction of young arteries.
41                       Our findings show that endothelium-dependent control of swine coronary artery t
42 tment is effective in partial restoration of endothelium-dependent coronary flow.
43 n the collateral dependent region, preserves endothelium-dependent coronary vessel function, and upre
44       This allows the combined assessment of endothelium-dependent (CPT) and endothelium-independent
45 osine hydroxylase-positive axon density) and endothelium-dependent dilatation (carbachol) of the MCA
46                                              Endothelium-dependent dilatation (ED) is abnormal in pat
47 aerobic exercise is associated with enhanced endothelium-dependent dilatation (EDD) in older humans,
48             Acetylcholine (ACh)-induced peak endothelium-dependent dilatation (EDD) was lower in isol
49                                              Endothelium-dependent dilatation (EDD), assessed by the
50 ximately 30% (P <0.05) reduction in arterial endothelium-dependent dilatation (EDD).
51 anism involved in the age-related decline in endothelium-dependent dilatation (EDD).
52                  Spontaneous vasomotor tone, endothelium-dependent dilatation and adrenergic vasocons
53                         Acetylcholine caused endothelium-dependent dilatation that was decreased in o
54                        Heat therapy improved endothelium-dependent dilatation, arterial stiffness, in
55 y vascular endothelial dysfunction (impaired endothelium-dependent dilatation, EDD) and aortic stiffe
56 cular endothelial dysfunction (e.g. impaired endothelium-dependent dilatation, EDD).
57  protective endothelial functions, including endothelium-dependent dilatation.
58 ctase inhibitors (statins) improve cutaneous endothelium-dependent dilatation; however, whether stati
59  term high-fat diet feeding had no effect on endothelium dependent dilation.
60                       Ex vivo carotid artery endothelium-dependent dilation (EDD) to increasing doses
61 al function, as indicated in part by reduced endothelium-dependent dilation (EDD).
62 e inhibitor (apocynin), or anti-TNF restored endothelium-dependent dilation in Lepr(db) mice.
63 bitor (apocynin), or anti-TNF-alpha restored endothelium-dependent dilation in the ZOF rats.
64                                              Endothelium-dependent dilation is mediated by the releas
65 ere no sex differences in either NO-mediated endothelium-dependent dilation or endothelium-independen
66  the control diet, the HM/LF diet diminished endothelium-dependent dilation to 10 micromol/L acetylch
67 ioglitazone treatment significantly improved endothelium-dependent dilation to bradykinin (P=0.01) wi
68                                              Endothelium-dependent dilation was blunted in MDD and me
69                                     Finally, endothelium-dependent dilation was lower (P < 0.01) in i
70 ion (n=8; 7 women; 19-37 years), NO-mediated endothelium-dependent dilation was preserved, but endoth
71 sion of these NAD(P)H subunits and abrogated endothelium-dependent dilation.
72               Vascular endothelial function (endothelium-dependent dilation; EDD), nitric oxide (NO)/
73 t sympathetic vasoconstriction competes with endothelium-dependent dilator activity to determine post
74 VC) to local intra-arterial infusion of ACh (endothelium-dependent dilator) during resting conditions
75 ure to high glucose has a concentration- and endothelium-dependent effect on the myogenic tone of rat
76 ear-activated Kir currents and inhibition of endothelium-dependent flow-induced vasodilatation (FIV)
77  and 30 normotensive control subjects during endothelium-dependent flow-mediated dilatation induced b
78 o measure changes in segmental lumen volume (endothelium-dependent function).
79 ) venous occlusion plethysmography to assess endothelium-dependent (% Hyper) and endothelium-independ
80 re sites of dynamic Ca(2+) events leading to endothelium dependent hyperpolarization (EDH)-mediated r
81 esenteric arteries the K(Ca)2.3 component of endothelium-dependent hyperpolarization (EDH) is lost fo
82                 To further study the role of endothelium-dependent hyperpolarization (EDH), ACh trial
83 ions and limits the impact of the disease on endothelium-dependent hyperpolarization (EDH)-mediated v
84 ) channels serve as electrical amplifiers of endothelium-dependent hyperpolarization (EDH).
85                We propose that initiation of endothelium-dependent hyperpolarization is the underlyin
86 xation of vascular smooth muscle through the endothelium-dependent hyperpolarizing factor (EDHF) path
87 helium independent) and acetylcholine (ACh) (endothelium dependent) iontophoresis, flicker-light-indu
88 ascular superoxide and H2O2 production in an endothelium-dependent manner and elicited a concentratio
89 ferent physiologic or pharmacologic stimuli, endothelium-dependent (micro)vascular reactivity can be
90 he index of microvascular resistance; third, endothelium-dependent microvascular function assessment
91            In men, the HF F&V diet increased endothelium-dependent microvascular reactivity (P = 0.01
92                                              Endothelium-dependent microvascular relaxation response
93                              The response to endothelium-dependent microvascular vasodilation was gre
94                                              Endothelium-dependent microvessel relaxation was moderat
95 d stable basal tone and the vasodilations to endothelium-dependent nitric oxide (NO)-mediated agonist
96  The authors examined whether CRP can affect endothelium-dependent nitric oxide (NO)-mediated dilatio
97  of CRP (7 microg/mL; 60 minutes) attenuated endothelium-dependent nitric oxide-mediated and prostacy
98  on the effects of aging and hypertension on endothelium-dependent nitric oxide-mediated vasodilation
99               We sought to determine whether endothelium-dependent NO regulates TG2 activity by S-nit
100 nificantly attenuated arteriolar dilation to endothelium-dependent NO-mediated agonists bradykinin an
101                                 CRP inhibits endothelium-dependent NO-mediated dilation in retinal ar
102  direct evidence for selective impairment of endothelium-dependent NO-mediated dilation of retinal ar
103                                              Endothelium-dependent NO-mediated dilation of retinal ar
104 nder normal conditions through constraint of endothelium-dependent NO-mediated vasodilatation in heal
105                                          The endothelium-dependent NO-mediated vasodilations to brady
106                                 By impairing endothelium-dependent NO-mediated vasoreactivity, CRP ca
107                Simvastatin elicits mainly an endothelium-dependent, NO-mediated dilation of retinal a
108 ial fluid, with emphasis on whether they are endothelium dependent or O(2) dependent.
109                                  CRP elicits endothelium-dependent oxidative stress and compromises n
110 olecular mechanisms underlying the pulmonary endothelium-dependent protective effects of APN.
111 his is the first study in humans to identify endothelium-dependent regulation of sympathetic vasocons
112 cellular signaling mechanism responsible for endothelium-dependent regulation of vascular smooth musc
113  ability of vascular rings to respond to the endothelium-dependent relaxant acetylcholine, both durin
114                                              Endothelium-dependent relaxation (EDR) is an initial key
115 ic tone was significantly potentiated, while endothelium-dependent relaxation (EDR) was impaired in s
116 38 prevented NADP(H) depletion and preserved endothelium-dependent relaxation and NO generation with
117 t to diabetes mellitus-induced impairment in endothelium-dependent relaxation and reendothelializatio
118 cids and GLP-1 were associated with improved endothelium-dependent relaxation compared with sham-oper
119  In addition, impaired acetylcholine-induced endothelium-dependent relaxation could be related to dec
120 2-CreNox2KO mice, along with preservation of endothelium-dependent relaxation during angiotensin II s
121 significantly improved acetylcholine-induced endothelium-dependent relaxation in AMPKalpha2(-/-) mice
122 ion of l-sepiapterin normalized the impaired endothelium-dependent relaxation in aortas isolated from
123 ease in STIM1 protein expression, attenuates endothelium-dependent relaxation in diabetic coronary ar
124  stress and SERCA oxidation and improved the endothelium-dependent relaxation in isolated mouse aorta
125 lose inspection reveals a specific effect on endothelium-dependent relaxation in mesenteric resistanc
126                    We also observed impaired endothelium-dependent relaxation in resistant vessels fr
127 e control, exhibited striking improvement in endothelium-dependent relaxation in response to acetylch
128                                              Endothelium-dependent relaxation in response to shear st
129         Functionally, acetylcholine-induced, endothelium-dependent relaxation is impaired in T1DM mes
130 pid accumulation in the liver; and decreased endothelium-dependent relaxation of aorta.
131 reduced ejection fraction, mitral E/A ratio, endothelium-dependent relaxation of coronary arteries, t
132 emporal profile of Ca(2+) dynamics underlies endothelium-dependent relaxation of swine coronary arter
133 re no acute changes in BP or the NO-mediated endothelium-dependent relaxation of the brachial artery
134  the Ca(2+) concentration in the ER, and (3) endothelium-dependent relaxation that was attenuated in
135                                              Endothelium-dependent relaxation was enhanced in male CF
136       Vasodilator prostanoid contribution to endothelium-dependent relaxation was reduced in lobar ar
137 ared to the wild type, acetylcholine-induced endothelium-dependent relaxation was significantly impai
138 heterozygout mice (db/m) mice and effects on endothelium-dependent relaxation, insulin sensitivity, a
139 ha release, and improved coronary arteriolar endothelium-dependent relaxation.
140  arteries and the role played by caveolae in endothelium-dependent relaxation.
141 ae structure and integrity are essential for endothelium-dependent relaxation.
142 hereas, in pregnant rats, PVAT-media reduced endothelium-dependent relaxation.
143 ed with decreased NO production and impaired endothelium-dependent relaxation.
144 ich restored NO bioavailability and improved endothelium-dependent relaxations and HDL endothelium-pr
145                                     Impaired endothelium-dependent relaxations in renal arteries, car
146  mice exhibited an accelerated impairment of endothelium-dependent relaxations in response to in vitr
147                                 Hcy impaired endothelium-dependent relaxations of rat aortae and led
148 ived hyperpolarizing factor (EDHF)-mediated, endothelium-dependent relaxations of small mesenteric ar
149 helium-independent and prostacyclin-mediated endothelium-dependent relaxations were not changed.
150 gh glucose in vitro induced an impairment of endothelium-dependent relaxations, which was prevented b
151 ction, which is characterized by an impaired endothelium-dependent response to vasodilators and hyper
152 the alteration in neurovascular coupling and endothelium-dependent responses in somatosensory cortex
153                                              Endothelium-dependent responses to acetylcholine in pres
154 a-arterial infusion of ACh or ATP to augment endothelium-dependent signalling during exercise attenua
155 dy, we tested the hypothesis that increasing endothelium-dependent signalling during exercise in olde
156                    In this study, increasing endothelium-dependent signalling during exercise signifi
157                     However, augmentation of endothelium-dependent signalling via infusion of ACh or
158 exercise + infusion of ACh or ATP to augment endothelium-dependent signalling.
159 monstrate that, given a sufficient stimulus, endothelium-dependent sympatholysis remains intact in ol
160 ver, H(2)O(2) has never been shown to be the endothelium-dependent transferrable hyperpolarization fa
161 peraldosteronism is associated with impaired endothelium-dependent vascular reactivity owing to incre
162 contributes, at least partially, to impaired endothelium-dependent vascular relaxation and hypertensi
163                  oxLDL-induced impairment of endothelium-dependent vascular relaxation of vascular ri
164 riments from mice showed that L5 compromised endothelium-dependent vascular relaxation through a nitr
165 ild and moderate HHcy aggravated HG-impaired endothelium-dependent vascular relaxation to acetylcholi
166 xposure of WKY rat aortas to IL-17F impaired endothelium-dependent vascular relaxation, whereas IL-17
167 hat this mechanism is important in impairing endothelium-dependent vascular relaxation.
168 mental role in regulating endothelial NO and endothelium-dependent vascular tone by deacetylating eNO
169 lationship between the two in the context of endothelium-dependent vascular tone is unknown.
170                  Nor-NOHA markedly increased endothelium-dependent vasodilatation (up to 2-fold) in p
171                                       Higher endothelium-dependent vasodilatation by ACh or leptin wa
172 ilure Assessment score, leukocyte count, and endothelium-dependent vasodilatation conferred an increa
173 ctional hyperaemia are reduced with age, and endothelium-dependent vasodilatation declines with age i
174 ance (HOMA-IR), was associated with impaired endothelium-dependent vasodilatation in FH- (p < 0.03, a
175 related increases in oxidative stress impair endothelium-dependent vasodilatation in humans, leading
176 termine whether arginase activity diminishes endothelium-dependent vasodilatation in skeletal muscle
177 rginine completely inhibited the increase in endothelium-dependent vasodilatation induced by nor-NOHA
178 e results demonstrate that the impairment of endothelium-dependent vasodilatation induced by old age
179                We hypothesized that impaired endothelium-dependent vasodilatation is a predictor of m
180                In vivo bedside assessment of endothelium-dependent vasodilatation is an independent p
181  potassium (Kir) channels, but their role in endothelium-dependent vasodilatation is not clear.
182                                              Endothelium-dependent vasodilatation is reduced with adv
183 sine triphosphate release and stimulation of endothelium-dependent vasodilatation may explain impairm
184                               Ageing reduces endothelium-dependent vasodilatation through an endothel
185                                           An endothelium-dependent vasodilatation value of 0.5% or le
186 hat contracting muscle selectively amplifies endothelium-dependent vasodilatation via activation of K
187                                              Endothelium-dependent vasodilatation was calculated as t
188                                              Endothelium-dependent vasodilatation was impaired in cor
189                                              Endothelium-dependent vasodilatation was impaired in hig
190 annel function was not altered, although the endothelium-dependent vasodilatation was severely impair
191             In logistic regression analysis, endothelium-dependent vasodilatation was the only predic
192 adrenergic-induced vasoconstriction, reduced endothelium-dependent vasodilatation, and enhanced hypox
193 ostatic conditions demonstrated a decline in endothelium-dependent vasodilatation, but restored the f
194  probably due (in part) to an improvement in endothelium-dependent vasodilatation.
195 airment of coronary blood flow responses and endothelium-dependent vasodilatation.
196 nnels, thereby causing hyperpolarization and endothelium-dependent vasodilatation.
197                                              Endothelium-dependent vasodilatations in response to mus
198                                   It induces endothelium dependent vasodilation, but the precise rece
199  The extract possesses the ability to induce endothelium dependent vasodilation, which is dependent o
200 tolerance and brachial artery flow-mediated, endothelium-dependent vasodilation (EDV) were assessed i
201    Almonds, compared with control, increased endothelium-dependent vasodilation (mean difference 4.1%
202                                The change in endothelium-dependent vasodilation achieved with fasudil
203 IRT1 in the endothelium of arteries inhibits endothelium-dependent vasodilation and decreases bioavai
204 active hyperemic index (RHI), which measures endothelium-dependent vasodilation and is a surrogate ma
205             Here we show that SIRT1 promotes endothelium-dependent vasodilation by targeting endothel
206 ng-severe systolic hypertension and impaired endothelium-dependent vasodilation due to uncoupled NO s
207 MA levels and reduce nitric oxide levels and endothelium-dependent vasodilation in a murine model and
208                            Fasudil increased endothelium-dependent vasodilation in CAD subjects from
209 pressure in healthy individuals and improves endothelium-dependent vasodilation in obese and overweig
210      Indeed, both flow-mediated dilation and endothelium-dependent vasodilation in response to acetyl
211                                     Impaired endothelium-dependent vasodilation is a hallmark of obes
212  determine whether putative modifications in endothelium-dependent vasodilation of the principal nutr
213 glutathionylation is increased with impaired endothelium-dependent vasodilation that is restored by t
214 One mechanistic hypothesis involves impaired endothelium-dependent vasodilation through reactive oxyg
215 histocompatibility complex class I inhibited endothelium-dependent vasodilation to acetylcholine.
216 de for a possible coupling mechanism linking endothelium-dependent vasodilation to bone remodeling.
217              mCMV-ND mice exhibited impaired endothelium-dependent vasodilation versus mock-ND at 9 a
218                                          PNA endothelium-dependent vasodilation was assessed in vitro
219                                     Coronary endothelium-dependent vasodilation was examined by infus
220 on was associated with larger improvement in endothelium-dependent vasodilation) (r=-0.48; P=0.01).
221 diabetic mice exhibited a marked decrease in endothelium-dependent vasodilation, a modest decrease in
222 s an important determinant of eNOS coupling, endothelium-dependent vasodilation, and superoxide produ
223 ysfunction, we measured endothelial markers, endothelium-dependent vasodilation, arteriolar glycocaly
224  placebo, allopurinol significantly improved endothelium-dependent vasodilation, by both forearm veno
225 LRs on endothelial cells leading to impaired endothelium-dependent vasodilation, increased vascular t
226 (*-) generation, is associated with impaired endothelium-dependent vasodilation.
227 pothesis that Ca(2+) influx via TRPA1 causes endothelium-dependent vasodilation.
228 n, including Ca(2+) signaling, integrity and endothelium-dependent vasodilation.
229 rate for nitric oxide synthesis, and impairs endothelium-dependent vasodilation.
230 ange in augmentation index in response to an endothelium-dependent vasodilator (salbutamol).
231 nses to intra-arterial administration of the endothelium-dependent vasodilator acetylcholine (P=0.03)
232       Coronary blood flow in response to the endothelium-dependent vasodilator acetylcholine as well
233 d by neural activity, hypercapnia, or by the endothelium-dependent vasodilator acetylcholine.
234 n but did not ameliorate the response to the endothelium-dependent vasodilator acetylcholine.
235 alpha(1) -agonist) during (i) infusion of an endothelium-dependent vasodilator alone (Protocol 1: ACh
236 /min), SLIGKV (160 to 800 nmol/min), and the endothelium-dependent vasodilator bradykinin (100 to 100
237      Similar to Ercc1(d/-) mice, age-related endothelium-dependent vasodilator dysfunction in Xpd(TTD
238  response to norepinephrine, and an impaired endothelium-dependent vasodilator response to acetylchol
239 on and no impairments in vasoconstrictor and endothelium-dependent vasodilator responses, associated
240                    Elevation of IP(3) by the endothelium-dependent vasodilator, acetylcholine, increa
241 absolute forearm blood-flow responses to the endothelium-dependent vasodilator, acetylcholine, increa
242 cid (LPA) has been recognized recently as an endothelium-dependent vasodilator, but several lines of
243 ) were calculated during (1) infusion of the endothelium-dependent vasodilators acetylcholine (ACh) a
244 ion responses of precontracted arterioles to endothelium-dependent vasodilators adenosine 5'-diphosph
245 blood flow elicited by neural activity or by endothelium-dependent vasodilators in WT mice but not in
246 IK(Ca)/SK(Ca)), NS309 (10(-5) M), and to the endothelium-dependent vasodilators, substance P (10(-8)
247                                              Endothelium-dependent vasodilators, such as acetylcholin
248 itric oxide bioavailability at rest and with endothelium-dependent vasodilators.
249 t K(IR) channels function as 'amplifiers' of endothelium-dependent vasodilators.
250  endothelial intracellular [Ca(2+)] regulate endothelium-dependent vasodilatory pathways, the molecul
251                  In young adults, increasing endothelium-dependent vasodilatory signalling during mil
252 first in humans to demonstrate that specific endothelium-dependent vasodilatory signalling is amplifi
253 etal muscle contractions selectively amplify endothelium-dependent vasodilatory signalling via activa
254    We tested the hypothesis that stimulating endothelium-dependent vasodilatory signalling will enhan
255  1.0 [0.9-1.0], P<0.001), and displayed less endothelium-dependent vasomotion (% change segmental lum
256 Per2, a circadian gene, is known to regulate endothelium-dependent vasomotion.
257 X-1 contributes to adverse effects of CRP on endothelium-dependent vasomotor function in resistance a
258                                              Endothelium-dependent vasomotor function, as measured by
259  identify p53 as an important determinant of endothelium-dependent vasomotor function.
260      Thus, the relationship between coronary endothelium-dependent vasomotor reactivity and atheroma
261 icate that endothelial Rac1 is essential for endothelium-dependent vasomotor response and ischemia-in
262                  5-MTHF improved NO-mediated endothelium-dependent vasomotor responses and reduced va
263     However, the role of SIRT1 in regulating endothelium-dependent vasomotor tone is not known.
264 can partially restore the normal response to endothelium-dependent vasorelaxants and myocardial perfu
265 ditions, Sirt1(endo-/-) mice showed impaired endothelium-dependent vasorelaxation and angiogenesis, a
266 ary arteries, sCD40L significantly decreased endothelium-dependent vasorelaxation and eNOS mRNA level
267 temic antagonism of miR-204 rescues impaired endothelium-dependent vasorelaxation and vascular Sirt1,
268                               Improvement of endothelium-dependent vasorelaxation by antibiotics is l
269 s in vitro, confirming that ceramide impairs endothelium-dependent vasorelaxation in a tissue-autonom
270 nificantly improved myocardial perfusion and endothelium-dependent vasorelaxation in chronically isch
271 her also improved vascular H(4)B content and endothelium-dependent vasorelaxation in diabetes.
272 vailable vascular nitric oxide, and improves endothelium-dependent vasorelaxation in mouse aortas.
273 o reduce systemic blood pressure and improve endothelium-dependent vasorelaxation in patients with at
274 ) and the 3-plex significantly also impaired endothelium-dependent vasorelaxation in response to brad
275                                              Endothelium-dependent vasorelaxation in response to brad
276  RAAS inhibition normalized MAP and improved endothelium-dependent vasorelaxation in sGCalpha1-defici
277  release, at least partly contributes to the endothelium-dependent vasorelaxation induced by the KATP
278 onses in resistance arteries and facilitates endothelium-dependent vasorelaxation only when CO(2)/HCO
279    Collectrin knockout mice display impaired endothelium-dependent vasorelaxation that is associated
280  downregulated endothelial Cav1 and impaired endothelium-dependent vasorelaxation that was rescued by
281  endothelial dysfunction measured by blunted endothelium-dependent vasorelaxation to acetylcholine, w
282  endothelial dysfunction measured by blunted endothelium-dependent vasorelaxation to acetylcholine, w
283                                      Maximal endothelium-dependent vasorelaxation to BK (bradykinin;
284                                              Endothelium-dependent vasorelaxation was impaired in you
285 malization, blunted ROS production, restored endothelium-dependent vasorelaxation, and attenuated apo
286 arrow endothelial progenitor cells, improved endothelium-dependent vasorelaxation, and markedly delay
287 elial nitric oxide synthase (eNOS), impaired endothelium-dependent vasorelaxation, and mild hypertens
288 othelial ER stress, associated impairment of endothelium-dependent vasorelaxation, and preserves endo
289 tigates angiotensin II-induced impairment of endothelium-dependent vasorelaxation, decrease in bioava
290 dothelial dysfunction, signalled by impaired endothelium-dependent vasorelaxation, is an early marker
291 ss of type I IFN receptor signaling improved endothelium-dependent vasorelaxation, lipoprotein parame
292  administration markedly attenuated impaired endothelium-dependent vasorelaxation, SERCA oxidation, E
293 tion, and rescue decline of aortic Sirt1 and endothelium-dependent vasorelaxation, triggered by high-
294 cg1(-/-) mice exhibited a marked decrease in endothelium-dependent vasorelaxation, while Abca1(-/-) m
295 ent increase in blood pressure, and impaired endothelium-dependent vasorelaxation.
296 e, insulin-mediated glucose utilization, and endothelium-dependent vasorelaxation.
297 al membrane potential and play a key role in endothelium-dependent vasorelaxation.
298 es in the regulation of vasoconstriction and endothelium-dependent vasorelaxation.
299 R-204 expression, reduced Cav1, and impaired endothelium-dependent vasorelaxation.
300 chanical stress, and its knock-down inhibits endothelium-dependent vasorelaxation.

 
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