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Nitric oxide and endothelium-derived hyperpolarizing factor: formation and interactions
J Bauersachs1, R Popp, I Fleming
1Zentrum der Physiologie, Klinikum der Johann Wolfgang Goethe-Universität, Frankfurt am Main, Germany.
Prostaglandins, Leukotrienes, and Essential Fatty Acids
|January 16, 1998
Summary
This study reveals a new mechanism for endothelial nitric oxide synthase (eNOS) activation by shear stress, independent of calcium. It also shows nitric oxide (NO) inhibits endothelium-derived hyperpolarizing factor (EDHF) production.
Area of Science:
- Vascular biology
- Endothelial function
- Autacoid signaling
Background:
- Endothelial autacoids, nitric oxide (NO) and endothelium-derived hyperpolarizing factor (EDHF), regulate vascular tone.
- Existing knowledge on NO and EDHF pathways controlling vascular tone is incomplete.
Purpose of the Study:
- To elucidate a novel pathway for endothelial NO synthase (eNOS) activation.
- To investigate the interaction between NO and EDHF formation.
Main Methods:
- Investigated calcium-independent eNOS activation via shear stress and tyrosine phosphorylation.
- Characterized EDHF as a P450-dependent arachidonic acid metabolite.
- Examined the inhibitory effect of NO on EDHF production.
Main Results:
- Identified a novel pathway for calcium-independent eNOS activation by shear stress and tyrosine phosphorylation.
- Demonstrated that NO inhibits EDHF formation.
- Characterized EDHF as a transferable, beta-naphthoflavone-inducible P450-dependent metabolite of arachidonic acid.
Conclusions:
- Shear stress activates eNOS through a calcium-independent pathway involving tyrosine phosphorylation.
- Nitric oxide plays an inhibitory role in the synthesis of EDHF.
- Understanding these pathways is crucial for controlling vascular tone.