Endothelium-dependent contractions in hypertension.
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.
Vanhoutte
Paul M
PM
Department of Pharmacology, Faculty of Medicine, University of Hong Kong, Hong Kong, China. vanhoutte.hku@hku.hk
Feletou
Michel
M
Taddei
Stefano
S
D000818:Animals; D004730:Endothelium, Vascular / Q000503:physiopathology*; D006801:Humans; D006973:Hypertension / Q000503:physiopathology*; D009119:Muscle Contraction / Q000502:physiology*; D009131:Muscle, Smooth, Vascular / Q000503:physiopathology*; D014664:Vasodilation / Q000502:physiology*