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1 ulate the release of the endothelium-derived relaxing factor.
2 um to cause synthesis of endothelium-derived relaxing factor.
3 to influence release of endothelium-derived relaxing factor.
4 members of the family of endothelium-derived relaxing factors.
6 NO) is identified as the endothelium-derived relaxing factor and a neurotransmitter with a superfusio
7 e degradation of NO, the endothelium-derived relaxing factor and a primary mediator of endothelial fu
8 considered an important endothelium-derived relaxing factor and may function to protect blood vessel
9 ide radical can scavenge endothelium-derived relaxing factor and produce potent oxidizing agents, whi
10 e biological activity of endothelium-derived relaxing factor and that this decrease can be reversed b
11 The identification of endothelium-derived relaxing factor as nitric oxide (NO) dramatically altere
13 sporine, wortmannin, the endothelium-derived relaxing factor congener S-nitroso-N-acetylcysteine (SNA
15 sitive, and synthesis of endothelial-derived relaxing factor (EDRF), therefore, may be most important
17 n the endothelium (e.g., endothelium-derived relaxing factor, endothelium-derived hyperpolarizing fac
19 dulin, eNOS produces NO, endothelial-derived relaxing factor, from l-arginine (l-Arg) by means of ele
20 ally active component of endothelium-derived relaxing factor, has critical roles in the maintenance o
22 cardiac tissue, is known to act as a soluble relaxing factor in fast skeletal muscle fibers by acting
24 iscover and identify new endothelium-derived relaxing factors involved in the regulation of erectile
26 ght to determine whether endothelium-derived relaxing factor (nitric oxide) exerts a tonic vasodilati
27 oxide synthase-dependent endothelium-derived relaxing factor response and paradoxically enhances cont
28 orelaxant effects of the endothelium-derived relaxing factor S-nitrosocysteine (SNC) may not be simpl
29 hat NO is the prototypic endothelium-derived relaxing factor, this signaling molecule was implicated
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