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Endothelium‐dependent contractions: when a good guy turns bad!
Author(s) -
Vanhoutte Paul M.,
Tang Eva H. C.
Publication year - 2008
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2008.161430
Subject(s) - prostacyclin , endothelium , nitric oxide , endocrinology , medicine , vasodilation , chemistry , thromboxane , thromboxane a2 , cyclooxygenase , vascular smooth muscle , prostanoid , endothelial dysfunction , intracellular , endothelium derived hyperpolarizing factor , receptor , biochemistry , smooth muscle , platelet , enzyme , charybdotoxin
Endothelial cells can induce contractions of the underlying vascular smooth muscle by generating vasoconstrictor prostanoids (endothelium‐dependent contracting factor; EDCF). The endothelial COX‐1 isoform of cyclooxygenase appears to play the dominant role in the phenomenon. Its activation requires an increase in intracellular Ca 2+ concentration. The production of EDCF is inhibited acutely and chronically by nitric oxide (NO), and possibly by endothelium‐dependent hyperpolarizing factor (EDHF). The main prostanoids involved in endothelium‐dependent contractions appear to be endoperoxides (PGH 2 ) and prostacyclin, which activate thromboxane‐prostanoid (TP) receptors of the vascular smooth muscle cells. Oxygen‐derived free radicals can facilitate the production and/or the action of EDCF. Endothelium‐dependent contractions are exacerbated by ageing, obesity, hypertension and diabetes, and thus are likely to contribute to the endothelial dysfunction observed in older people and in essential hypertensive patients.