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Article: EDHF: New therapeutic targets?

TitleEDHF: New therapeutic targets?
Authors
Issue Date2004
PublisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/issn/10436618
Citation
Pharmacological Research, 2004, v. 49 n. 6, p. 565-580 How to Cite?
AbstractBesides cyclooxygenase and NO-synthase, another distinct endothelial pathway, endothelium-dependent hyperpolarization (EDHF), is involved in the relaxation of the vascular smooth muscle cells. EDHF has been demonstrated unequivocally in various blood vessels from different species, including human, and is likely to play an important role in cardiovascular physiology. This alternative pathway involves the activation of two populations of endothelial potassium channels, the small conductance and intermediate conductance calcium-activated potassium channels (SKCa and IKCa, respectively). EDHF-mediated responses are clearly altered in various pathological conditions (ageing, hypertension, atherosclerosis, hypercholesterolemia, heart failure, ischemia-reperfusion, angioplasty, eclampsia, diabetes, sepsis). Therapeutic or adjutant interventions (angiotensin converting enzyme inhibitors, antagonist of the angiotensin receptor, estrogen, omega-3 polyunsaturated fatty acids, polyphenol derivatives, potassium and/or calcium intake) can restore these responses, suggesting that the improvement of the EDHF pathway contributes to the observed beneficial effect of these various substances. However, the improvement or restoration of EDHF responses has not been, yet, the direct purpose of any pharmaceutical effort. Activating endothelial IKCa and/or SKCa or increasing their expression as well as improving myo-endothelial communication, for instance by increasing the expression of connexin(s), could become interesting therapeutic targets. © 2004 Elsevier Ltd. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/80279
ISSN
2015 Impact Factor: 4.816
2015 SCImago Journal Rankings: 2.108
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorFélétou, Men_HK
dc.contributor.authorVanhoutte, PMen_HK
dc.date.accessioned2010-09-06T08:04:32Z-
dc.date.available2010-09-06T08:04:32Z-
dc.date.issued2004en_HK
dc.identifier.citationPharmacological Research, 2004, v. 49 n. 6, p. 565-580en_HK
dc.identifier.issn1043-6618en_HK
dc.identifier.urihttp://hdl.handle.net/10722/80279-
dc.description.abstractBesides cyclooxygenase and NO-synthase, another distinct endothelial pathway, endothelium-dependent hyperpolarization (EDHF), is involved in the relaxation of the vascular smooth muscle cells. EDHF has been demonstrated unequivocally in various blood vessels from different species, including human, and is likely to play an important role in cardiovascular physiology. This alternative pathway involves the activation of two populations of endothelial potassium channels, the small conductance and intermediate conductance calcium-activated potassium channels (SKCa and IKCa, respectively). EDHF-mediated responses are clearly altered in various pathological conditions (ageing, hypertension, atherosclerosis, hypercholesterolemia, heart failure, ischemia-reperfusion, angioplasty, eclampsia, diabetes, sepsis). Therapeutic or adjutant interventions (angiotensin converting enzyme inhibitors, antagonist of the angiotensin receptor, estrogen, omega-3 polyunsaturated fatty acids, polyphenol derivatives, potassium and/or calcium intake) can restore these responses, suggesting that the improvement of the EDHF pathway contributes to the observed beneficial effect of these various substances. However, the improvement or restoration of EDHF responses has not been, yet, the direct purpose of any pharmaceutical effort. Activating endothelial IKCa and/or SKCa or increasing their expression as well as improving myo-endothelial communication, for instance by increasing the expression of connexin(s), could become interesting therapeutic targets. © 2004 Elsevier Ltd. All rights reserved.en_HK
dc.languageengen_HK
dc.publisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/issn/10436618en_HK
dc.relation.ispartofPharmacological Researchen_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshBiological Factors - agonists - antagonists & inhibitors - metabolismen_HK
dc.subject.meshDrug Delivery Systems - methodsen_HK
dc.subject.meshEndothelium, Vascular - drug effects - enzymology - metabolismen_HK
dc.subject.meshHumansen_HK
dc.subject.meshVascular Diseases - drug therapy - enzymology - metabolismen_HK
dc.titleEDHF: New therapeutic targets?en_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1043-6618&volume=49&spage=565&epage=580&date=2004&atitle=EDHF:+new+therapeutic+targets?en_HK
dc.identifier.emailVanhoutte, PM: vanhoutt@hku.hken_HK
dc.identifier.authorityVanhoutte, PM=rp00238en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.phrs.2003.10.017en_HK
dc.identifier.pmid15026034-
dc.identifier.scopuseid_2-s2.0-1542512300en_HK
dc.identifier.hkuros88060en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-1542512300&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume49en_HK
dc.identifier.issue6en_HK
dc.identifier.spage565en_HK
dc.identifier.epage580en_HK
dc.identifier.isiWOS:000221557000008-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridFélétou, M=7006461826en_HK
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_HK

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