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1 for how hydrogen peroxide can operate as an endothelium-derived hyperpolarizing factor.
2 sent a marker for the endothelial effects of endothelium-derived hyperpolarizing factor.
3 e vasodilatory properties similar to that of endothelium-derived hyperpolarizing factor.
4 Hence, like EETs, DHETs may function as endothelium-derived hyperpolarizing factors.
6 (e.g., endothelium-derived relaxing factor, endothelium-derived hyperpolarizing factor, and prostagl
7 nd epoxyeicosatrienoic acid release and that endothelium-derived hyperpolarizing factors compensate f
8 on in VHF rats, and blunted prostacyclin and endothelium-derived hyperpolarizing factor components in
12 ch as acetylcholine release an unidentified, endothelium-derived hyperpolarizing factor (EDHF) which
13 r relaxation is mediated by nitric oxide and endothelium-derived hyperpolarizing factor (EDHF), and b
14 is remaining vasorelaxation activity, termed endothelium-derived hyperpolarizing factor (EDHF), is mo
15 prostanoids, but involves the release of an endothelium-derived hyperpolarizing factor (EDHF), possi
16 l compounds, including prostacyclin, NO, and endothelium-derived hyperpolarizing factor (EDHF), that
17 (NO) synthase or K(+) channels that mediate endothelium-derived hyperpolarizing factor (EDHF)-depend
18 we investigated and compared NO release and endothelium-derived hyperpolarizing factor (EDHF)-mediat
19 severe HHcy impaired nitric oxide (NO)- and endothelium-derived hyperpolarizing factor (EDHF)-mediat
25 potassium ion (K(+)) have been identified as endothelium-derived hyperpolarizing factors (EDHFs) in a
26 nd hydrogen peroxide (H2O2) both function as endothelium-derived hyperpolarizing factors (EDHFs) in t
27 on of vascular smooth muscle are mediated by endothelium-derived hyperpolarizing factors (EDHFs).
28 y cytochrome P-450 monooxygenase (P450), are endothelium-derived hyperpolarizing factors (EDHFs).
30 ified C-type natriuretic peptide (CNP) as an endothelium-derived hyperpolarizing factor in the mesent
31 ioisomers, which were recently identified as endothelium-derived hyperpolarizing factors in coronary
32 like" SKA-31 (half-life of 12 h) potentiated endothelium-derived hyperpolarizing factor-mediated dila
33 n endothelial cells to produce nitric oxide, endothelium-derived hyperpolarizing factor, or prostagla
34 r-dependent effects on NO, prostacyclin, and endothelium-derived hyperpolarizing factor production, t
35 l cell surface contributes to control of the endothelium-derived hyperpolarizing factor response, alt
38 hanism contributes to the effects of EETs as endothelium-derived hyperpolarizing factors to hyperpola
40 ctivating TEA-inhibitable K(+)(Ca) channels, endothelium-derived hyperpolarizing factors, together wi
41 effects of nitric oxide, prostaglandins, and endothelium-derived hyperpolarizing factor were inhibite
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