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Endothelial dysfunction: a multifaceted disorder (The Wiggers Award Lecture).
Endothelial cells synthesize and release various factors that regulate angiogenesis, inflammatory responses, hemostasis, as well as vascular tone and permeability. Endothelial dysfunction has been
Endothelium-derived hyperpolarising factors and associated pathways: a synopsis
The term endothelium-derived hyperpolarising factor (EDHF) was introduced in 1987 to describe the hypothetical factor responsible for myocyte hyperpolarisations not associated with nitric oxide
Endothelium-Derived Hyperpolarizing Factor: Where Are We Now?
TLDR
The endothelium controls vascular tone not only by releasing nitric oxide and prostacyclin but also by other pathways causing hyperpolarization of the underlying smooth muscle cells, which can be evoked by direct electrical coupling through myo-endothelial junctions and/or the accumulation of potassium ions in the intercellular space.
Acetylcholine‐induced endothelium‐dependent contractions in the SHR aorta: the Janus face of prostacyclin
TLDR
In the aorta of SHR and aging WKY, the endothelium‐dependent contractions elicited by acetylcholine most likely involve the release of PGI2 with a concomitant contribution of PGH2.
Endothelial dysfunction and vascular disease
TLDR
The endothelium can evoke relaxations (dilatations) of the underlying vascular smooth muscle, by releasing vasodilator substances, which are reduced in the course of vascular disease and selectively loose the pertussis toxin‐sensitive pathway for NO release which favours vasospasm, thrombosis, penetration of macrophages, cellular growth and the inflammatory reaction leading to atherosclerosis.
Endothelium‐mediated control of vascular tone: COX‐1 and COX‐2 products
TLDR
Since in most cases, the activation of TP receptors is the common downstream effector, selective antagonists of this receptor should curtail endothelial dysfunction and be of therapeutic interest in the treatment of cardiovascular disorders.
Endothelium‐dependent hyperpolarization of canine coronary smooth muscle
TLDR
It is suggested that endothelium‐derived relaxing factor(s) induces hyperpolarization of vascular smooth muscle of the canine coronary artery, possibly by activation of sodium‐potassium pumping, but that this effect on the cell membrane may only partially explain endot helium‐dependent relaxations evoked by acetylcholine.
Endothelium‐dependent contractions in hypertension
TLDR
Since EDCF causes vasoconstriction by activation of the TP‐receptors on the vascular smooth muscle cells, selective antagonists at these receptors prevent endothelium‐dependent contractions, and curtail the endothelial dysfunction in hypertension and diabetes.
Endothelial dysfunction and vascular disease – a 30th anniversary update
TLDR
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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