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Article: Is endothelin involved in the pathogenesis of hypertension?

TitleIs endothelin involved in the pathogenesis of hypertension?
Authors
Issue Date1993
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://hyper.ahajournals.org/
Citation
Hypertension, 1993, v. 21 n. 6 I, p. 747-751 How to Cite?
AbstractEndothelins are a family of potent vasoconstrictor peptides released by endothelial cells. The production of endothelin-1 (ET-1) can be stimulated by aggregating platelets and angiotensin II. It is inhibited by increases in intracellular concentration of cyclic GMP. ET-1 causes biphasic changes in arterial blood pressure and of peripheral resistance in several vascular beds: an initial transient decrease (due to release of nitric oxide, prostacyclin, or both from the endothelium) followed by a sustained increase (mainly due to direct activation of vascular smooth muscle). The vasoconstriction induced by the peptide is inhibited by increases in cyclic GMP. Few studies, except in pregnant women with preeclampsia or eclampsia, indicate that the circulating levels of the peptide are augmented in hypertension. Likewise, the information available on changes in responsiveness to endothelins in blood vessels from hypertensive animals is controversial. Until the effect of selective antagonists on the production or action of the peptide can be determined in hypertensive patients, caution must be exerted when implying a role for endothelin in the pathophysiology of hypertension.
Persistent Identifierhttp://hdl.handle.net/10722/171088
ISSN
2015 Impact Factor: 6.294
2015 SCImago Journal Rankings: 3.702
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:12:09Z-
dc.date.available2012-10-30T06:12:09Z-
dc.date.issued1993en_US
dc.identifier.citationHypertension, 1993, v. 21 n. 6 I, p. 747-751en_US
dc.identifier.issn0194-911Xen_US
dc.identifier.urihttp://hdl.handle.net/10722/171088-
dc.description.abstractEndothelins are a family of potent vasoconstrictor peptides released by endothelial cells. The production of endothelin-1 (ET-1) can be stimulated by aggregating platelets and angiotensin II. It is inhibited by increases in intracellular concentration of cyclic GMP. ET-1 causes biphasic changes in arterial blood pressure and of peripheral resistance in several vascular beds: an initial transient decrease (due to release of nitric oxide, prostacyclin, or both from the endothelium) followed by a sustained increase (mainly due to direct activation of vascular smooth muscle). The vasoconstriction induced by the peptide is inhibited by increases in cyclic GMP. Few studies, except in pregnant women with preeclampsia or eclampsia, indicate that the circulating levels of the peptide are augmented in hypertension. Likewise, the information available on changes in responsiveness to endothelins in blood vessels from hypertensive animals is controversial. Until the effect of selective antagonists on the production or action of the peptide can be determined in hypertensive patients, caution must be exerted when implying a role for endothelin in the pathophysiology of hypertension.en_US
dc.languageengen_US
dc.publisherLippincott Williams & Wilkins. The Journal's web site is located at http://hyper.ahajournals.org/en_US
dc.relation.ispartofHypertensionen_US
dc.subject.meshAnimalsen_US
dc.subject.meshBlood Pressure - Drug Effectsen_US
dc.subject.meshEndothelins - Blood - Pharmacology - Physiologyen_US
dc.subject.meshHumansen_US
dc.subject.meshHypertension - Etiologyen_US
dc.titleIs endothelin involved in the pathogenesis of hypertension?en_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.doi10.1161/01.HYP.21.6.747-
dc.identifier.pmid8500854-
dc.identifier.scopuseid_2-s2.0-0027241826en_US
dc.identifier.volume21en_US
dc.identifier.issue6 Ien_US
dc.identifier.spage747en_US
dc.identifier.epage751en_US
dc.identifier.isiWOS:A1993LF39200001-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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