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Endothelium‐dependent contractions in hypertension
Author(s) -
Vanhoutte Paul M,
Feletou Michel,
Taddei Stefano
Publication year - 2005
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1038/sj.bjp.0706042
Subject(s) - vasoconstriction , endothelium , endocrinology , medicine , vascular smooth muscle , vasodilation , nitric oxide , angiotensin ii , contraction (grammar) , superoxide , endothelin receptor , endothelial dysfunction , chemistry , receptor , endothelins , endothelium derived relaxing factor , smooth muscle , biochemistry , enzyme
1 Endothelial cells, under given circumstances, can initiate contraction (constriction) of the vascular smooth muscle cells that surround them. Such endothelium‐dependent, acute increases in contractile tone can be due to the withdrawal of the production of nitric oxide, to the production of vasoconstrictor peptides (angiotensin II, endothelin‐1), to the formation of oxygen‐derived free radicals (superoxide anions) and/or the release of vasoconstrictor metabolites of arachidonic acid. The latter have been termed endothelium‐derived contracting factor (EDCF) as they can contribute to moment‐to‐moment changes in contractile activity of the underlying vascular smooth muscle cells. 2 To judge from animal experiments, EDCF‐mediated responses are exacerbated by aging, spontaneous hypertension and diabetes. 3 To judge from human studies, they contribute to the blunting of endothelium‐dependent vasodilatations in aged subjects and essential hypertensive patients. 4 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.British Journal of Pharmacology (2005) 144 , 449–458. doi: 10.1038/sj.bjp.0706042