The endothelium plays an important role in maintaining vascular homeostasis by synthesizing and releasing several vasodilating factors, including prostacyclin, nitric oxide, and endothelium-derived hyperpolarizing factor (EDHF). We have recently identified that endothelium-derived hydrogen peroxide (H2O2) is an EDHF in mice. The present study was designed to examine whether this is also the case in humans. Bradykinin elicited endothelium-dependent relaxations and hyperpolarizations in the presence of indomethacin and Nω-nitro-L-arginine, which thus were attributed to EDHF, in human mesenteric arteries. The EDHF-mediated relaxations were significantly inhibited by catalase, an enzyme that specifically decomposes H2O2, whereas catalase did not affect endothelium-independent hyperpolarizations to levcromakalim. Exogenous H2O2 elicited relaxations and hyperpolarizations in endothelium-stripped arteries. Gap junction inhibitor 18α-glycyrrhetinic acid partially inhibited, whereas inhibitors of cytochrome P450 did not affect the EDHF-mediated relaxations. These results indicate that H2O2 is also a primary EDHF in human mesenteric arteries with some contribution of gap junctions.
|Number of pages||5|
|Journal||Biochemical and Biophysical Research Communications|
|Publication status||Published - Jan 1 2002|
All Science Journal Classification (ASJC) codes
- Molecular Biology
- Cell Biology