1 very of endothelium-derived relaxing factor (EDRF) and its importance in the identification of nitric

2 esis of endothelial-derived relaxing factor (EDRF), therefore, may be most important in these vessels

3  and/or endothelium-derived relaxing factor (EDRF)/NO.

4                              After 72 hours, EDRF/NO was assessed from acetylcholine-induced, NO synt

5 nal vessels, indicating that the increase in EDRF may nullify direct Ang II-induced vasoconstriction.

6                       The characteristics of EDRF, when released from endothelial cells, were similar

7                         A major component of EDRF activity derives from hyperpolarization and is term

8      Hydrogen sulfide (H(2)S) is a prominent EDRF, since mice lacking its biosynthetic enzyme, cystat

9 helium-derived and eNOS-mediated relaxation (EDRF) is coupled to increased protein S-nitrosylation in

10 very labile, nonprostanoid substance, termed EDRF, that acted on vascular smooth muscle cells to acti

11                   It is now established that EDRF, either as NO or some related nitrosyl substance, h

12  [mean+/-SD] nmol x L(-1); P<0.005), whereas EDRF/NO responses and NO activity were not changed consi

13 lism in the kidney cortex and liver, whereas EDRF/NO is regulated primarily by DDAH-2, which is expre