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1 al NOS (eNOS) activity, and in aortic rings, endothelium-derived and eNOS-mediated relaxation (EDRF)
2 ecanoate (4alpha-PDD) (5 micromol/L) and the endothelium-derived arachidonic acid metabolite 11,12 ep
3         Epoxyeicosatrienoic acids (EETs) are endothelium-derived arachidonic acid metabolites of cyto
4 lcium-activated potassium channels (KCa) and endothelium-derived autacoids to CVD.
5 We confirm that TG2 activity is modulated by endothelium-derived bioactive NO in young rat aorta.
6                     We then demonstrate that endothelium-derived bioactive NO primarily mediates its
7 poxic pulmonary vasculature and suggest that endothelium-derived BMP4 plays a direct, paracrine role
8 ated by those that do not; (iii) PQ inhibits endothelium-derived, but not NO-induced, relaxations of
9 an mass in the legs and higher levels of the endothelium-derived C-terminal-pro-endothelin-1 (both p
10 hese results demonstrate a novel function of endothelium-derived Cat S in angiogenesis.
11           A combination of prothrombin time, endothelium-derived CD105-microparticles, and platelet c
12 thelial cells, aortic endothelial cells, and endothelium-derived cell line (ECV304).
13 s both resting and stimulated HUVEC, and the endothelium-derived chemokine CCL2 (monocyte chemoattrac
14        To date, however, the contribution of endothelium-derived chemokines found in these lesion to
15                                  We measured endothelium-derived clotting factors and assayed platele
16                                              Endothelium-derived CNP is involved in the regulation of
17      In contrast, TGF-beta1 did not decrease endothelium-derived constitutive NOS mRNA in organs of r
18                        Estrogen also affects endothelium-derived constrictor factors.
19 cessive primary tumor growth but depended on endothelium-derived EETs at the site of metastasis.
20 tion of these routes is determined by venous endothelium-derived endothelin-1, acting through its spe
21                                              Endothelium-derived epoxyeicosatrienoic acids (EETs) rel
22       Further characterization revealed that endothelium-derived EVs (EC-EVs) suppressed monocyte act
23  Researchers recently found elevated pigment endothelium-derived factor (PEDF) associated with active
24 rived Vegf-A, and identify Hgf as a putative endothelium-derived factor that mediates the reciprocal
25 rmation and suggesting that Hgf serves as an endothelium-derived factor that signals to the epitheliu
26 ations to bradykinin by increased release of endothelium-derived factors other than nitric oxide.
27 endothelium with a higher mitotic index than endothelium derived from local sources.
28 ndings indicate novel potential functions of endothelium-derived GABA.
29                                              Endothelium-derived gene products play a critical role i
30                                        Thus, endothelium-derived HS chains and mast cell-derived hepa
31 responses were instead abolished by blocking endothelium derived hyperpolarising factor (EDHF) with a
32 rate that 10 mM propionate relaxes RMSAs via endothelium-derived hyperpolarising factor (EDHF).
33      These localized Ca(2+) events result in endothelium-derived hyperpolarization (and SMC relaxatio
34   Evidence from animal models has identified endothelium-derived hyperpolarization (EDH) as a potenti
35                  In striking contrast to the endothelium-derived hyperpolarization (EDH) characterist
36  arteries, RA-2 inhibited bradykinin-induced endothelium-derived hyperpolarization (EDH)-type relaxat
37 ATPase in humans, consistent with a role for endothelium-derived hyperpolarization in functional symp
38  present in arterial endothelium to generate endothelium-derived hyperpolarization.
39                                 Dilations to endothelium-derived hyperpolarizing factor (EDHF) are si
40                    It has been proposed that endothelium-derived hyperpolarizing factor (EDHF) contri
41 ch as acetylcholine release an unidentified, endothelium-derived hyperpolarizing factor (EDHF) which
42 r relaxation is mediated by nitric oxide and endothelium-derived hyperpolarizing factor (EDHF), and b
43 is remaining vasorelaxation activity, termed endothelium-derived hyperpolarizing factor (EDHF), is mo
44  prostanoids, but involves the release of an endothelium-derived hyperpolarizing factor (EDHF), possi
45 l compounds, including prostacyclin, NO, and endothelium-derived hyperpolarizing factor (EDHF), that
46  (NO) synthase or K(+) channels that mediate endothelium-derived hyperpolarizing factor (EDHF)-depend
47  we investigated and compared NO release and endothelium-derived hyperpolarizing factor (EDHF)-mediat
48  severe HHcy impaired nitric oxide (NO)- and endothelium-derived hyperpolarizing factor (EDHF)-mediat
49 gen peroxide (H2O2), which is proposed as an endothelium-derived hyperpolarizing factor (EDHF).
50 relaxations that are widely attributed to an endothelium-derived hyperpolarizing factor (EDHF).
51 l toxins reported to block the release of an endothelium-derived hyperpolarizing factor (EDHF).
52 derives from hyperpolarization and is termed endothelium-derived hyperpolarizing factor (EDHF).
53 crucial component of dilation resulting from endothelium-derived hyperpolarizing factor (EDHF).
54                               Thus, enhanced endothelium-derived hyperpolarizing factor activity in c
55 on in VHF rats, and blunted prostacyclin and endothelium-derived hyperpolarizing factor components in
56           This is consistent with a role for endothelium-derived hyperpolarizing factor in FID of the
57 ified C-type natriuretic peptide (CNP) as an endothelium-derived hyperpolarizing factor in the mesent
58 r-dependent effects on NO, prostacyclin, and endothelium-derived hyperpolarizing factor production, t
59 l cell surface contributes to control of the endothelium-derived hyperpolarizing factor response, alt
60 effects of nitric oxide, prostaglandins, and endothelium-derived hyperpolarizing factor were inhibite
61  increased involvement of prostaglandins and endothelium-derived hyperpolarizing factor(s).
62 ently by enhanced production of the putative endothelium-derived hyperpolarizing factor(s).
63  (e.g., endothelium-derived relaxing factor, endothelium-derived hyperpolarizing factor, and prostagl
64 n endothelial cells to produce nitric oxide, endothelium-derived hyperpolarizing factor, or prostagla
65 like" SKA-31 (half-life of 12 h) potentiated endothelium-derived hyperpolarizing factor-mediated dila
66 sent a marker for the endothelial effects of endothelium-derived hyperpolarizing factor.
67 e vasodilatory properties similar to that of endothelium-derived hyperpolarizing factor.
68  for how hydrogen peroxide can operate as an endothelium-derived hyperpolarizing factor.
69 potassium ion (K(+)) have been identified as endothelium-derived hyperpolarizing factors (EDHFs) in a
70 nd hydrogen peroxide (H2O2) both function as endothelium-derived hyperpolarizing factors (EDHFs) in t
71 on of vascular smooth muscle are mediated by endothelium-derived hyperpolarizing factors (EDHFs).
72 y cytochrome P-450 monooxygenase (P450), are endothelium-derived hyperpolarizing factors (EDHFs).
73 nd epoxyeicosatrienoic acid release and that endothelium-derived hyperpolarizing factors compensate f
74                         We hypothesized that endothelium-derived hyperpolarizing factors contribute t
75 ioisomers, which were recently identified as endothelium-derived hyperpolarizing factors in coronary
76 hanism contributes to the effects of EETs as endothelium-derived hyperpolarizing factors to hyperpola
77              We assessed the contribution of endothelium-derived hyperpolarizing factors to resting a
78 ctivating TEA-inhibitable K(+)(Ca) channels, endothelium-derived hyperpolarizing factors, together wi
79      Hence, like EETs, DHETs may function as endothelium-derived hyperpolarizing factors.
80 time points (2-8 hours) after AECA addition, endothelium-derived interleukin-1 (IL-1) accounted for t
81  residual responses were mediated by another endothelium-derived mediator or NO released despite trea
82 ia-cell injury may result in an imbalance in endothelium-derived mediators, favouring vasoconstrictio
83  act by inducing the release of at least two endothelium-derived mediators, one (as-yet-unidentified)
84 take place in the occlusive lesions and that endothelium-derived mesenchymal cells can further differ
85  salt rats were resistant to the blocking of endothelium derived nitric oxide (EDNO) with L-NAME and
86  rabbits, oral L-arginine (the substrate for endothelium derived nitric oxide) attenuates endothelial
87 fts has been attributed in part to increased endothelium-derived nitric oxide (.NO) production.
88                                      Loss of endothelium-derived nitric oxide (EDNO) contributes to t
89                      The effective action of endothelium-derived nitric oxide (EDNO) is impaired in p
90  endothelium-dependent vasodilator function, endothelium-derived nitric oxide (EDNO) production, and
91 y a role in the modulation of the release of endothelium-derived nitric oxide (EDNO).
92 n action and vasodilation may be mediated by endothelium-derived nitric oxide (EDNO).
93 portant for shear stress-mediated release of endothelium-derived nitric oxide (NO) and lowering pulmo
94                                      Loss of endothelium-derived nitric oxide (NO) and prostacyclin c
95                We tested the hypothesis that endothelium-derived nitric oxide (NO) and vasodilating p
96  a key role in the endogenous suppression of endothelium-derived nitric oxide (NO) bioactivity and ha
97                                              Endothelium-derived nitric oxide (NO) contributes to epi
98           Ageing is associated with impaired endothelium-derived nitric oxide (NO) function in human
99 bination of other nutrients known to enhance endothelium-derived nitric oxide (NO) in patients with s
100                                              Endothelium-derived nitric oxide (NO) is a potent vasodi
101                                              Endothelium-derived nitric oxide (NO) is an important re
102                                              Endothelium-derived nitric oxide (NO) is an important re
103 ntal stress-induced vasodilation mediated by endothelium-derived nitric oxide (NO) is defective in co
104                                              Endothelium-derived nitric oxide (NO) is synthesised fro
105                                              Endothelium-derived nitric oxide (NO) may be an importan
106               The reduced bioavailability of endothelium-derived nitric oxide (NO) may play a role in
107                           The bioactivity of endothelium-derived nitric oxide (NO) reflects its rates
108                                              Endothelium-derived nitric oxide (NO) selectively enhanc
109                                              Endothelium-derived nitric oxide (NO) selectively enhanc
110              Many angiogenic factors require endothelium-derived nitric oxide (NO) to exert their eff
111          Cerebral blood flow is regulated by endothelium-derived nitric oxide (NO), and endothelial N
112 flow is a potent stimulus for the release of endothelium-derived nitric oxide (NO).
113  mutations affect vasorelaxation mediated by endothelium-derived nitric oxide (NO).
114  taken during hand hyperemia (a stimulus for endothelium-derived nitric oxide [NO] release in the ups
115 .47 mN/mm; P=0.004) attributable to impaired endothelium-derived nitric oxide activity.
116 ssociated with atherosclerosis by preserving endothelium-derived nitric oxide activity.
117             In particular, the production of endothelium-derived nitric oxide and activation of solub
118 e (ADMA), correlate with decreased levels of endothelium-derived nitric oxide and subsequent endothel
119 at is likely to be related to a reduction in endothelium-derived nitric oxide bioavailability and/or
120 gh a mechanism that is not caused by loss of endothelium-derived nitric oxide but may involve oxidati
121                              Inactivation of endothelium-derived nitric oxide by oxygen-derived free
122          Oxidatively mediated degradation of endothelium-derived nitric oxide contributes to abnormal
123                                              Endothelium-derived nitric oxide contributes to basal sy
124 is investigation sought to determine whether endothelium-derived nitric oxide contributes to hypoxia-
125                                              Endothelium-derived nitric oxide contributes to systemic
126 stress is associated with impaired action of endothelium-derived nitric oxide in patients with athero
127 dy was undertaken to investigate the role of endothelium-derived nitric oxide in the regulation of fo
128 nthase (Nos3), which suggests that decreased endothelium-derived nitric oxide is not a sufficient mec
129 rovide a mechanism by which FXR may increase endothelium-derived nitric oxide levels through modulati
130                    Decreased availability of endothelium-derived nitric oxide may contribute to the h
131               The reduced bioavailability of endothelium-derived nitric oxide may play a role in endo
132          There are some data indicating that endothelium-derived nitric oxide mediates changes in vas
133            To study the effect of endogenous endothelium-derived nitric oxide on TF expression and ac
134                     Oxidative degradation of endothelium-derived nitric oxide plays a major role in e
135 ese data suggest that enhanced production of endothelium-derived nitric oxide reduces endotoxin- and
136                               Stimulation of endothelium-derived nitric oxide with acetylcholine resu
137 ndothelium-dependent relaxation (mediated by endothelium-derived nitric oxide) is depressed during th
138               L-arginine is the precursor of endothelium-derived nitric oxide, an endogenous vasodila
139 n molecules and decreased bioavailability of endothelium-derived nitric oxide, an important regulator
140                       Hemoglobin inactivates endothelium-derived nitric oxide, participates in free-r
141 sodilates skeletal muscle vasculature via an endothelium-derived nitric oxide-dependent mechanism.
142 nt mechanism whereby hyperglycemia decreases endothelium-derived nitric oxide.
143 e endothelial dysfunction: essential role of endothelium-derived nitric oxide.
144 ized by a decrease in the bioavailability of endothelium-derived nitric oxide.
145 ial artery cannula to assess vasodilation to endothelium-derived nitric oxide.
146 sodilator function that depends partially on endothelium-derived nitric oxide.
147 structural and functional factors, including endothelium-derived nitric oxide.
148 d cANF(4-23) were enhanced in the absence of endothelium-derived nitric oxide.
149                                     Although endothelium derived NO has been shown to be of prime imp
150 at estradiol may stimulate the production of endothelium-derived NO and thereby reduce the contractil
151                                 Both p21 and endothelium-derived NO appear to have protective roles i
152 -coupled receptor-mediated, or shear-induced endothelium-derived NO bioactivity) is understood to inv
153 d antioxidant status has been shown to alter endothelium-derived NO bioactivity.
154 d the role of intracellular ascorbic acid in endothelium-derived NO bioactivity.
155                                              Endothelium-derived NO controls the contractility and gr
156                                              Endothelium-derived NO has been shown to be of crucial i
157                                              Endothelium-derived NO is considered to be primarily an
158                                          The endothelium-derived NO is detected amperometrically at a
159 nvolve, at least in part, the attenuation of endothelium-derived NO production through a calcineurin-
160 may protect against vasospasm by stimulating endothelium-derived NO release and inhibiting coronary a
161                 In these cells, VEGF and the endothelium-derived NO synergistically up-regulated the
162 nation reaction of plasma oxyhemoglobin with endothelium-derived NO to form bioinactive nitrate.
163 nyl thiol redox switch to decrease pulmonary endothelium-derived NO(.) and promote PAH.
164 ions of bradykinin, a well-known stimulus of endothelium-derived NO, activated nitric oxide synthase
165  hypertrophy through the paracrine action of endothelium-derived NO, which triggers the degradation o
166 e contributes to impairment of the action of endothelium-derived NO.
167 onstriction via the possible facilitation of endothelium-derived NO.
168 that this effect of exercise is meditated by endothelium-derived NO.
169 tivation, with apparently less of a role for endothelium-derived NO.
170  vascular endothelium as a result of loss of endothelium-derived NO.
171 d in part by .O2-, likely via degradation of endothelium-derived NO.
172 t exert its action through direct effects on endothelium-derived NO.
173 nd resistance vessels is mediated in part by endothelium-derived NO.
174 reases the production and bioavailability of endothelium-derived NO.
175 it refractoriness and repriming depends upon endothelium-derived NO.
176 poxanthine/xanthine oxidase system inhibited endothelium-derived .NO-mediated arterial relaxation eli
177                            However, although endothelium-derived PDGF-BB appears vital for the develo
178                                          The endothelium-derived peptide endothelin-1 (ET-1) causes v
179                    Endothelin-1 (ET-1) is an endothelium-derived peptide that constricts coronary ves
180 ciated with increased expression of ET-1, an endothelium-derived peptide with vasoconstricting, mitog
181                     We tested the role of an endothelium-derived phosphatidylserine-binding opsonin,
182                      The vasomotor effect of endothelium-derived prostacyclin was examined by monitor
183 portant physiological platelet inhibitors is endothelium-derived prostacyclin which stimulates the pl
184 ulated release and proteolytic processing of endothelium-derived Reelin.
185 isolated arteries, focusing our attention on endothelium-derived relaxation and on its antioxidant pr
186  within the current framework of NO biology, endothelium-derived relaxation factor activity (ie, G pr
187    Well over 2 decades have passed since the endothelium-derived relaxation factor was reported to be
188 y, imbalance in the relative contribution of endothelium-derived relaxing and contracting factors, an
189                             The discovery of endothelium-derived relaxing factor (EDRF) and its impor
190  or -2 regulates serum ADMA (S(ADMA)) and/or endothelium-derived relaxing factor (EDRF)/NO.
191               We sought to determine whether endothelium-derived relaxing factor (nitric oxide) exert
192       Nitric oxide (NO) is identified as the endothelium-derived relaxing factor and a neurotransmitt
193 he production and the degradation of NO, the endothelium-derived relaxing factor and a primary mediat
194 nitric oxide (NO) is considered an important endothelium-derived relaxing factor and may function to
195          The superoxide radical can scavenge endothelium-derived relaxing factor and produce potent o
196 e (Hcy) decreases the biological activity of endothelium-derived relaxing factor and that this decrea
197                        The identification of endothelium-derived relaxing factor as nitric oxide (NO)
198 cular endothelium accounts in large part for endothelium-derived relaxing factor bioactivity.
199 taglandin I2, staurosporine, wortmannin, the endothelium-derived relaxing factor congener S-nitroso-N
200  an impaired nitric oxide synthase-dependent endothelium-derived relaxing factor response and paradox
201              The vasorelaxant effects of the endothelium-derived relaxing factor S-nitrosocysteine (S
202                                        As an endothelium-derived relaxing factor, a mediator of immun
203 by signals arising in the endothelium (e.g., endothelium-derived relaxing factor, endothelium-derived
204 e (NO), the biologically active component of endothelium-derived relaxing factor, has critical roles
205 wing the discovery that NO is the prototypic endothelium-derived relaxing factor, this signaling mole
206 tes that pHi may modulate the release of the endothelium-derived relaxing factor.
207 act on the endothelium to cause synthesis of endothelium-derived relaxing factor.
208 have also been shown to influence release of endothelium-derived relaxing factor.
209                                  A number of endothelium-derived relaxing factors have been identifie
210  this study was to discover and identify new endothelium-derived relaxing factors involved in the reg
211 ienoic acids as new members of the family of endothelium-derived relaxing factors.
212 dependent on the addition of exogenous Zn2+, endothelium-derived S-SMase was partially active even in
213                  These factors will serve as endothelium derived signaling molecules in the tumor mic
214 ine mechanisms involving the upregulation of endothelium-derived stabilizing factors and the recruitm
215        Endothelial microparticles (EMPs) are endothelium-derived submicron vesicles that are released
216 indings have highlighted the contribution of endothelium-derived substances to blood flow control in
217 raction; local metabolic, red blood cell and endothelium-derived substances; and the sympathetic nerv
218              We recently identified TL1A, an endothelium-derived T cell costimulator and a ligand for
219 DAMTS-13, a metalloprotease that cleaves the endothelium-derived ultra-large multimers of von Willebr
220                    Endothelin-1 (ET-1) is an endothelium-derived vasoactive peptide with mitogenic pr
221                    Cyclooxygenase-dependent, endothelium-derived vasoconstrictor release modulates ac
222 ) influx, (2) the release (by hypoxia) of an endothelium-derived vasoconstrictor, or (3) endothelium-
223 ion is characterized by an imbalance between endothelium-derived vasodilating and vasoconstricting fa
224 increased intima/media ratio, and maintained endothelium-derived vasodilation.
225 hyporeactivity in large part mediated by the endothelium-derived vasodilator nitric oxide.
226  is that they improve the bioactivity of the endothelium-derived vasodilator NO by enhancing NO synth
227 entation of L-arginine, the precursor of the endothelium-derived vasodilator NO, reverses coronary en
228 drogen sulfide (H(2)S), a recently described endothelium-derived vasodilator, is produced by the enzy
229 constrictors, such as endothelin, antagonize endothelium-derived vasodilators and contribute to endot
230  Epoxyeicosatrienoic acids (EETs) are potent endothelium-derived vasodilators formed from cytochrome
231           In the present study, the roles of endothelium-derived vasodilators, guanylyl cyclase, and
232 ular tone of mouse cerebral arteries through endothelium-derived vasodilatory mechanisms.

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