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Conference Paper: Endothelium-dependent hyperpolarization: age, gender and high blood pressure, does it matter?

TitleEndothelium-dependent hyperpolarization: age, gender and high blood pressure, does it matter?
Authors
Issue Date2015
PublisherWiley-Blackwell Publishing Ltd. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=1748-1708
Citation
The 2015 Meeting of Endothelium-Dependent Hyperpolarizations in Health and Disease, Nyborg, Funen, Denmark, 14 -17 September 2015. In Acta Physiologica, 2015, v. 215 n. suppl. 703, p. 11, abstract no. 25 How to Cite?
AbstractVascular complications, such as atherosclerosis, develop with aging and hypertension. Female appears to have a lower risk of developing vascular diseases compared to age-matched male, until after menopause. Impairment of vascular function is associated with an impaired capacity of the endothelium to generate vasodilator signals, the major ones being nitric oxide (NO) and endothelium-dependent hyperpolarization (EDH). A reduction in the bioavailability of NO has been well documented with endothelial dysfunction. By contrast, although the contribution of EDH-like responses to the regulation of vascular tone increases as the diameter of the arteries decreases, the modulation of such relaxation by age, gender and hypertension is less clear. Whereas the mechanism involved in EDH-like relaxations varies with species and blood vessel types, activation of endothelial intermediate-and small-conductance calcium-activated potassium channels (IKCa and SKCa, respectively) are characteristic of this pathway. In superior mesenteric arteries of aged, hypertensive or post-menopausal atherosclerotic-prone rodents, EDH-type relaxations are reduced compared to those of preparations of respective controls. Pharmacological experiments in mesenteric arteries of hypertensive rats suggest a reduced involvement of SKCa, such that EDH-mediated relaxation becomes dependent on IKCa. This IKCa-mediated response appears to involve the activation of adenosine monophosphate-activated protein kinase (AMPK) and silent information regulator T1 (SIRT1), proteins associated with the process of cellular senescence and vascular signaling in response to female hormone. An understanding of the role of AMPK and/or SIRT1 in EDH-like responses may help identifying effective pharmacological strategies to prevent the development of vascular complications of different etiology.
DescriptionThis free journal suppl. entitled: Special Issue: Abstracts of the Meeting on Endothelium-Dependent Hyperpolarizations in Health and Disease, 14-17 Septmeber 2015, Nyborg, Denmark
Persistent Identifierhttp://hdl.handle.net/10722/229984
ISSN
2015 Impact Factor: 4.066
2015 SCImago Journal Rankings: 1.690

 

DC FieldValueLanguage
dc.contributor.authorLeung, SWS-
dc.contributor.authorVanhoutte, PM-
dc.date.accessioned2016-08-23T14:14:28Z-
dc.date.available2016-08-23T14:14:28Z-
dc.date.issued2015-
dc.identifier.citationThe 2015 Meeting of Endothelium-Dependent Hyperpolarizations in Health and Disease, Nyborg, Funen, Denmark, 14 -17 September 2015. In Acta Physiologica, 2015, v. 215 n. suppl. 703, p. 11, abstract no. 25-
dc.identifier.issn1748-1708-
dc.identifier.urihttp://hdl.handle.net/10722/229984-
dc.descriptionThis free journal suppl. entitled: Special Issue: Abstracts of the Meeting on Endothelium-Dependent Hyperpolarizations in Health and Disease, 14-17 Septmeber 2015, Nyborg, Denmark-
dc.description.abstractVascular complications, such as atherosclerosis, develop with aging and hypertension. Female appears to have a lower risk of developing vascular diseases compared to age-matched male, until after menopause. Impairment of vascular function is associated with an impaired capacity of the endothelium to generate vasodilator signals, the major ones being nitric oxide (NO) and endothelium-dependent hyperpolarization (EDH). A reduction in the bioavailability of NO has been well documented with endothelial dysfunction. By contrast, although the contribution of EDH-like responses to the regulation of vascular tone increases as the diameter of the arteries decreases, the modulation of such relaxation by age, gender and hypertension is less clear. Whereas the mechanism involved in EDH-like relaxations varies with species and blood vessel types, activation of endothelial intermediate-and small-conductance calcium-activated potassium channels (IKCa and SKCa, respectively) are characteristic of this pathway. In superior mesenteric arteries of aged, hypertensive or post-menopausal atherosclerotic-prone rodents, EDH-type relaxations are reduced compared to those of preparations of respective controls. Pharmacological experiments in mesenteric arteries of hypertensive rats suggest a reduced involvement of SKCa, such that EDH-mediated relaxation becomes dependent on IKCa. This IKCa-mediated response appears to involve the activation of adenosine monophosphate-activated protein kinase (AMPK) and silent information regulator T1 (SIRT1), proteins associated with the process of cellular senescence and vascular signaling in response to female hormone. An understanding of the role of AMPK and/or SIRT1 in EDH-like responses may help identifying effective pharmacological strategies to prevent the development of vascular complications of different etiology.-
dc.languageeng-
dc.publisherWiley-Blackwell Publishing Ltd. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=1748-1708-
dc.relation.ispartofActa Physiologica-
dc.rightsPreprint This is the pre-peer reviewed version of the following article: [FULL CITE], which has been published in final form at [Link to final article]. Authors are not required to remove preprints posted prior to acceptance of the submitted version. Postprint This is the accepted version of the following article: [full citation], which has been published in final form at [Link to final article].-
dc.titleEndothelium-dependent hyperpolarization: age, gender and high blood pressure, does it matter?-
dc.typeConference_Paper-
dc.identifier.emailLeung, SWS: swsleung@hku.hk-
dc.identifier.emailVanhoutte, PM: vanhoutt@hku.hk-
dc.identifier.authorityLeung, SWS=rp00235-
dc.identifier.authorityVanhoutte, PM=rp00238-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1111/apha.12558-
dc.identifier.hkuros262188-
dc.identifier.volume215-
dc.identifier.issuesuppl. 703-
dc.identifier.spage11, abstract no. 25-
dc.identifier.epage11, abstract no. 25-
dc.publisher.placeUnited Kingdom-

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