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Article: Endothelium-dependent contractions: From superoxide anions to TP-receptor agonists

TitleEndothelium-dependent contractions: From superoxide anions to TP-receptor agonists
Authors
KeywordsArachidonic Acid
Endoperoxide
Endothelin
Hypertension
Isoprostane
Nitric Oxide
Superoxide Anion
Thromboxane A2
Tp-Receptor
Issue Date2002
Citation
Dialogues In Cardiovascular Medicine, 2002, v. 7 n. 4, p. 211-222 How to Cite?
AbstractBesides causing relaxation of the underlying smooth muscle through the release of endothelium-derived relaxing factors (EDRFs), the endothelial cells of certain blood vessels, under given circumstances, can also trigger the contraction (constriction) of these muscle cells. Such acute, endothelium-dependent, increases in contractile tone can be due to the suppression of nitric oxide production (constitutive or stimulated), or to the production of vasoconstrictor peptides (angiotensin II or endothelin-1) or oxygen-derived free radicals (superoxide anions) and/or vasoconstrictor products of arachidonic acid metabolism (endoperoxides, thromboxane A2, and possibly isoprostanes). The latter have been termed endothelium-derived contracting factors (EDCFs) as they can contribute to moment-to-moment changes in contractile activity of the vascular smooth muscle cells that surround the endothelium from which they originate. EDCF-mediated responses are most pronounced in large cerebral arteries, and are enhanced by aging, spontaneous hypertension, and diabetes. They contribute to the blunting of endothelium-dependent vasodilations in aged subjects and subjects with essential hypertension. Since EDCFs cause contraction of vascular smooth muscle by activation of thromboxane-prostanoid (TP) receptors, selective antagonists at these receptors are able to prevent endothelium-dependent contractions, thus opening up prospects for potential therapeutic implications.
Persistent Identifierhttp://hdl.handle.net/10722/171294
ISSN
2015 SCImago Journal Rankings: 0.106
References

 

DC FieldValueLanguage
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:13:14Z-
dc.date.available2012-10-30T06:13:14Z-
dc.date.issued2002en_US
dc.identifier.citationDialogues In Cardiovascular Medicine, 2002, v. 7 n. 4, p. 211-222en_US
dc.identifier.issn1272-9949en_US
dc.identifier.urihttp://hdl.handle.net/10722/171294-
dc.description.abstractBesides causing relaxation of the underlying smooth muscle through the release of endothelium-derived relaxing factors (EDRFs), the endothelial cells of certain blood vessels, under given circumstances, can also trigger the contraction (constriction) of these muscle cells. Such acute, endothelium-dependent, increases in contractile tone can be due to the suppression of nitric oxide production (constitutive or stimulated), or to the production of vasoconstrictor peptides (angiotensin II or endothelin-1) or oxygen-derived free radicals (superoxide anions) and/or vasoconstrictor products of arachidonic acid metabolism (endoperoxides, thromboxane A2, and possibly isoprostanes). The latter have been termed endothelium-derived contracting factors (EDCFs) as they can contribute to moment-to-moment changes in contractile activity of the vascular smooth muscle cells that surround the endothelium from which they originate. EDCF-mediated responses are most pronounced in large cerebral arteries, and are enhanced by aging, spontaneous hypertension, and diabetes. They contribute to the blunting of endothelium-dependent vasodilations in aged subjects and subjects with essential hypertension. Since EDCFs cause contraction of vascular smooth muscle by activation of thromboxane-prostanoid (TP) receptors, selective antagonists at these receptors are able to prevent endothelium-dependent contractions, thus opening up prospects for potential therapeutic implications.en_US
dc.languageengen_US
dc.relation.ispartofDialogues in Cardiovascular Medicineen_US
dc.subjectArachidonic Aciden_US
dc.subjectEndoperoxideen_US
dc.subjectEndothelinen_US
dc.subjectHypertensionen_US
dc.subjectIsoprostaneen_US
dc.subjectNitric Oxideen_US
dc.subjectSuperoxide Anionen_US
dc.subjectThromboxane A2en_US
dc.subjectTp-Receptoren_US
dc.titleEndothelium-dependent contractions: From superoxide anions to TP-receptor agonistsen_US
dc.typeArticleen_US
dc.identifier.emailVanhoutte, PM:vanhoutt@hku.hken_US
dc.identifier.authorityVanhoutte, PM=rp00238en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.scopuseid_2-s2.0-0037772209en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0037772209&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume7en_US
dc.identifier.issue4en_US
dc.identifier.spage211en_US
dc.identifier.epage222en_US
dc.publisher.placeFranceen_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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