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Hydrogen peroxide is an endothelium-derived hyperpolarizing factor in human mesenteric arteries
Tetsuya Matoba1, Hiroaki Shimokawa, Hiroshi Kubota
1Department of Cardiovascular Medicine, Kyushu University Graduate School of Medical Sciences, Fukuoka, 812-8582, Japan.
Biochemical and Biophysical Research Communications
|January 19, 2002
Summary
Endothelium-derived hydrogen peroxide (H2O2) acts as a key endothelium-derived hyperpolarizing factor (EDHF) in human mesenteric arteries. This finding reveals a novel mechanism for vascular homeostasis and vasodilation in humans.
Area of Science:
- Cardiovascular Physiology
- Endothelial Function
- Molecular Biology
Background:
- The endothelium regulates vascular tone through vasodilators like nitric oxide and prostacyclin.
- Endothelium-derived hyperpolarizing factor (EDHF) is crucial for vascular homeostasis.
- Previous studies identified hydrogen peroxide (H2O2) as an EDHF in mice.
Purpose of the Study:
- To investigate if H2O2 functions as an EDHF in human mesenteric arteries.
- To elucidate the mechanisms underlying EDHF-mediated vasodilation in humans.
Main Methods:
- Human mesenteric arteries were used to study vasodilation and hyperpolarization.
- Pharmacological agents including indomethacin, N-omega-nitro-L-arginine, catalase, and gap junction inhibitors were employed.
- Endothelium-dependent and independent responses were assessed.
Main Results:
- Bradykinin induced endothelium-dependent relaxations and hyperpolarizations attributed to EDHF.
- Catalase significantly inhibited these EDHF-mediated responses, indicating H2O2's role.
- Exogenous H2O2 mimicked these effects, and gap junction inhibition partially attenuated the response.
Conclusions:
- Hydrogen peroxide (H2O2) is a primary endothelium-derived hyperpolarizing factor (EDHF) in human mesenteric arteries.
- H2O2 contributes significantly to endothelium-dependent vasodilation.
- Gap junctions play a partial role in H2O2-mediated vascular effects.