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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
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
13 s both resting and stimulated HUVEC, and the endothelium-derived chemokine CCL2 (monocyte chemoattrac
20 tion of these routes is determined by venous endothelium-derived endothelin-1, acting through its spe
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.
31 responses were instead abolished by blocking endothelium derived hyperpolarising factor (EDHF) with a
34 Evidence from animal models has identified endothelium-derived hyperpolarization (EDH) as a potenti
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
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
55 on in VHF rats, and blunted prostacyclin and endothelium-derived hyperpolarizing factor components in
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
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
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
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
78 ctivating TEA-inhibitable K(+)(Ca) channels, endothelium-derived hyperpolarizing factors, together wi
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
90 endothelium-dependent vasodilator function, endothelium-derived nitric oxide (EDNO) production, and
93 portant for shear stress-mediated release of endothelium-derived nitric oxide (NO) and lowering pulmo
96 a key role in the endogenous suppression of endothelium-derived nitric oxide (NO) bioactivity and ha
99 bination of other nutrients known to enhance endothelium-derived nitric oxide (NO) in patients with s
103 ntal stress-induced vasodilation mediated by endothelium-derived nitric oxide (NO) is defective in co
114 taken during hand hyperemia (a stimulus for endothelium-derived nitric oxide [NO] release in the ups
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
124 is investigation sought to determine whether endothelium-derived nitric oxide contributes to hypoxia-
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
135 ese data suggest that enhanced production of endothelium-derived nitric oxide reduces endotoxin- and
137 ndothelium-dependent relaxation (mediated by endothelium-derived nitric oxide) is depressed during th
139 n molecules and decreased bioavailability of endothelium-derived nitric oxide, an important regulator
141 sodilates skeletal muscle vasculature via an endothelium-derived nitric oxide-dependent mechanism.
150 at estradiol may stimulate the production of endothelium-derived NO and thereby reduce the contractil
152 -coupled receptor-mediated, or shear-induced endothelium-derived NO bioactivity) is understood to inv
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
162 nation reaction of plasma oxyhemoglobin with endothelium-derived NO to form bioinactive nitrate.
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
176 poxanthine/xanthine oxidase system inhibited endothelium-derived .NO-mediated arterial relaxation eli
180 ciated with increased expression of ET-1, an endothelium-derived peptide with vasoconstricting, mitog
183 portant physiological platelet inhibitors is endothelium-derived prostacyclin which stimulates the pl
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
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
196 e (Hcy) decreases the biological activity of endothelium-derived relaxing factor and that this decrea
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
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
210 this study was to discover and identify new endothelium-derived relaxing factors involved in the reg
212 dependent on the addition of exogenous Zn2+, endothelium-derived S-SMase was partially active even in
214 ine mechanisms involving the upregulation of endothelium-derived stabilizing factors and the recruitm
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
219 DAMTS-13, a metalloprotease that cleaves the endothelium-derived ultra-large multimers of von Willebr
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
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
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