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Eva Hoi Ching Tang
Researcher at Li Ka Shing Faculty of Medicine, University of Hong Kong
Publications - 23
Citations - 1819
Eva Hoi Ching Tang is an academic researcher from Li Ka Shing Faculty of Medicine, University of Hong Kong. The author has contributed to research in topics: Proinflammatory cytokine & Inflammation. The author has an hindex of 17, co-authored 23 publications receiving 1542 citations. Previous affiliations of Eva Hoi Ching Tang include Brigham and Women's Hospital & University of Hong Kong.
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Journal ArticleDOI
Endothelial dysfunction and vascular disease – a 30th anniversary update
TL;DR: It has become clear that nitric oxide itself, under certain conditions (e.g. hypoxia), can cause biased activation of soluble guanylyl cyclase leading to the production of cyclic inosine monophosphate rather than cGMP and hence causes contraction rather than relaxation of the underlying vascular smooth muscle.
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Gene expression changes of prostanoid synthases in endothelial cells and prostanoid receptors in vascular smooth muscle cells caused by aging and hypertension
TL;DR: The expression of prostacyclin synthase was by far the most abundant, explaining why the majority of the COX-1-derived endoperoxides are transformed into prostacy Clin, substantiating the role of prostACYclin as an endothelium-derived contracting factor.
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Endothelial dysfunction: a strategic target in the treatment of hypertension?
TL;DR: The severity of endothelial dysfunction correlates with the development of coronary artery disease and predicts future cardiovascular events as mentioned in this paper, and therefore, endothel dysfunction needs to be considered as a strategic target in the treatment of hypertension.
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Calcium and reactive oxygen species increase in endothelial cells in response to releasers of endothelium-derived contracting factor
Eva Hoi Ching Tang,Fung Ping Leung,Yu Huang,Michel Félétou,Kwok-Fai So,Ricky Y.K. Man,Paul M. Vanhoutte +6 more
TL;DR: Whether or not the intracellular concentration of calcium and reactive oxygen species (ROS) increase in endothelial cells of the rat thoracic aorta in response to releasers of endothelium‐derived contracting factor (EDCF) and if so, whether or not a difference exists between spontaneously hypertensive (SHR) and normotensive (WKY) rats.
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Endothelium-dependent contractions occur in the aorta of wild-type and COX2-/- knockout but not COX1-/- knockout mice.
Eva Hoi Ching Tang,David D. Ku,George L. Tipoe,Michel Félétou,Ricky Y.K. Man,Paul M. Vanhoutte +5 more
TL;DR: Direct evidence is provided that COX1 is indeed the isoform of cyclooxygenase responsible for the production of EDCF, and endothelium-dependent contractions in arteries of the mouse are revealed, as in the aorta of the spontaneously hypertensive rat.