Corpus ID: 21295775

Endothelial dysfunction and vascular disease.

@article{Vanhoutte1998EndothelialDA,
  title={Endothelial dysfunction and vascular disease.},
  author={Paul Michel Vanhoutte},
  journal={Verhandelingen - Koninklijke Academie voor Geneeskunde van Belgie},
  year={1998},
  volume={60 3},
  pages={
          251-66
        }
}
  • P. Vanhoutte
  • Published 1998
  • Medicine
  • Verhandelingen - Koninklijke Academie voor Geneeskunde van Belgie
The endothelium plays an obligatory role in a number of relaxations of isolated arteries. These endothelium-dependent relaxations are due to the release by the endothelial cells of potent vasodilator substances [endothelium-derived relaxing factors (EDRF)]. The best characterized EDRF is nitric oxide (NO). Nitric oxide is formed by the metabolism of L-arginine by the constitutive NO synthase of endothelial cells. In arterial smooth muscle, the relaxations evoked by EDRF are explained best by… Expand
Endothelial dysfunction and atherosclerosis.
TLDR
From animal studies it can be concluded that the propensity to release EDCFs is maintained, or even augmented, in diseased blood vessels, and the switch from a normally predominant release of EDRFs to that of ED CFs may play a crucial role in atherosclerosis. Expand
COX-mediated endothelium-dependent contractions: from the past to recent discoveries
TLDR
The present review summarizes and discusses the mechanisms leading to the release of EDCFs derived from the metabolism of arachidonic acid. Expand
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. Expand
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. Expand
Diverse Functions of Endothelial NO Synthases System: NO and EDH
TLDR
The diverse functions of endothelial NOSs system with NO and EDH/H2O2 could account for a compensatory mechanism in the setting of endothelium dysfunction. Expand
Endothelial control of vasomotor function: from health to coronary disease.
  • P. Vanhoutte
  • Medicine
  • Circulation journal : official journal of the Japanese Circulation Society
  • 2003
TLDR
This essay summarizes briefly the observations obtained mainly in the author’s laboratory that have determined how the secretion by endothelium cells of the relaxing factors underlies moment-to-moment changes in the tone of the surrounding vascular smooth muscle cells, and how the inability of the endothelial cells to do so eventually initiates atherosclerosis and thus vascular disease. Expand
Endothelium-Dependent Hyperpolarization and Endothelial Dysfunction
  • M. Félétou
  • Medicine
  • Journal of cardiovascular pharmacology
  • 2016
TLDR
A better characterization of EDH should allow determining whether new druggable targets can be identified for the treatment of cardiovascular diseases, as alteration of the EDH contributes to the endothelial dysfunctions observed in various pathologies or conversely compensates for the loss in NO bioavailability. Expand
Vascular biosynthesis of nitric oxide: effect on hemostasis and fibrinolysis.
  • V. Schini-Kerth
  • Medicine
  • Transfusion clinique et biologique : journal de la Societe francaise de transfusion sanguine
  • 1999
TLDR
The crucial role of vascular NO in the control of blood fluidity has been demonstrated by the regulation of the bleeding time in humans. Expand
G-protein-coupled receptor kinase 2 and endothelial dysfunction: molecular insights and pathophysiological mechanisms
TLDR
The pathophysiological mechanisms of insulin resistance and diabetes are described, focusing on the signal transduction for NO production via GRK2 and β-arrestin 2, providing novel insights into the potential field of translational investigation in the treatment of diabetic complications. Expand
Reversibility of endothelial dysfunction in diabetes: role of polyphenols.
TLDR
The role of polyphenolic compounds in modulating the differentially regulated pathways and thus maintaining vascular homeostasis has been proven to be beneficial. Expand
...
1
2
3
4
5
...