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Paul M. Vanhoutte

Researcher at University of Hong Kong

Publications -  868
Citations -  64681

Paul M. Vanhoutte is an academic researcher from University of Hong Kong. The author has contributed to research in topics: Endothelium & Vascular smooth muscle. The author has an hindex of 127, co-authored 868 publications receiving 62177 citations. Previous affiliations of Paul M. Vanhoutte include University of Rochester & University of Southern Denmark.

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Endothelium-derived relaxing and contracting factors.

TL;DR: Endothelium-dependent relaxation of blood vessels is produced by a large number of agents (e.g., acetylcholine, ATP and ADP, substance P, bradykinin, histamine, thrombin, serotonin). With some agents, relaxation may be limited to certain species and/or blood vessels as mentioned in this paper.
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Flow-induced release of endothelium-derived relaxing factor

TL;DR: It is demonstrated that in addition to prostacyclin, flow triggers the release of another relaxing substance (or substances) from vascular endothelial cells that has characteristics similar to the endothelium-derived relaxing factor released by acetylcholine.
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Superoxide anions and hyperoxia inactivate endothelium-derived relaxing factor.

TL;DR: It is demonstrated that superoxide anions inactivate the relaxing factor released by acetylcholine from endothelial cells and hyperoxia favors the inactivation of endothelium-derived relaxing factor(s).
Journal Article

Endothelium-derived relaxing and contracting factors.

TL;DR: Endothelium‐dependent relaxation of blood vessels is produced by a large number of agents (e.g., acetylcholine, ATP and ADP, substance P, bradykinin, histamine, thrombin, serotonin).
Journal ArticleDOI

Endothelial dysfunction in diabetes

TL;DR: Correcting the principal mediators of hyperglycaemia‐induced endothelial dysfunction may be activation of protein kinase C, increased activity of the polyol pathway, non‐enzymatic glycation and oxidative stress, as well as administration of ACE inhibitors and folate has been shown to improve endothelium‐dependent vasodilation in diabetes.