Abstract：
:Potassium channel dysfunction plays a role in the pathogenesis of a number of vascular diseases including pulmonary and systemic hypertension, diabetes, and complications of atherosclerosis. Two types of K+ channels that are known to be prevalent and contribute significantly to the repolarization of vascular smooth muscle cell (SMC) membranes are the high-conductance Ca(2+)- and voltage-activated K+ (BKCa) channels, and the voltage-gated K+ (KV) channels. Alterations in either BKCa or KV channel function can have dramatic effects on vascular tone. To date, hereditary and congenital mutations in genes encoding K+ channels, abnormalities in transcription, posttranslational modifications, and altered responses to intracellular second messengers have been described as potential mechanisms for several cardiovascular diseases. Comprehensive approaches including genetic, biochemical, molecular biological, and electrophysiological analyses are necessary to identify the levels at which K+ channel expression patterns or function are disrupted. Additionally, reproducing clinical pathologies in animal, organ, and virtual models has been important in studying the discrete mechanisms by which the structure and function of these channels are altered in pathophysiological conditions. This article will describe approaches that are currently used to identify abnormalities in BKCa and KV channels that may exist in diseases involving vascular dysfunction.
journal_name
Vascul Pharmacoljournal_title
Vascular pharmacologyauthors
Korovkina VP,England SKdoi
10.1016/s1537-1891(02)00121-0keywords:
subject
Has Abstractpub_date
2002-01-01 00:00:00pages
3-12issue
1eissn
1537-1891issn
1879-3649pii
S1537189102001210journal_volume
38pub_type
杂志文章,评审abstract：:Poorly controlled diabetes in pregnancy, characterized by hypo- and hyperglycemia, is associated with adverse outcomes. We hypothesized that aberrant glucose levels affect vascular function in pregnancy. The effects of glucose concentration on constriction and endothelium-dependent relaxation in uterine arteries of no...
journal_title：Vascular pharmacology
pub_type： 杂志文章
doi：10.1016/j.vph.2006.09.001
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journal_title：Vascular pharmacology
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doi：10.1016/j.vph.2005.03.005
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journal_title：Vascular pharmacology
pub_type： 杂志文章,评审
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journal_title：Vascular pharmacology
pub_type： 杂志文章,评审
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journal_title：Vascular pharmacology
pub_type： 杂志文章
doi：10.1016/j.vph.2018.07.001
更新日期：2018-11-01 00:00:00
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journal_title：Vascular pharmacology
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doi：10.1016/j.vph.2015.04.004
更新日期：2015-09-01 00:00:00
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journal_title：Vascular pharmacology
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journal_title：Vascular pharmacology
pub_type： 杂志文章
doi：10.1016/j.vph.2013.07.001
更新日期：2013-09-01 00:00:00
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journal_title：Vascular pharmacology
pub_type： 杂志文章
doi：10.1016/j.vph.2016.08.008
更新日期：2016-12-01 00:00:00
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journal_title：Vascular pharmacology
pub_type： 杂志文章,评审
doi：10.1016/j.vph.2011.08.224
更新日期：2011-10-01 00:00:00
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journal_title：Vascular pharmacology
pub_type： 杂志文章,meta分析,评审
doi：10.1016/j.vph.2015.09.005
更新日期：2016-05-01 00:00:00
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journal_title：Vascular pharmacology
pub_type： 杂志文章
doi：10.1016/s1537-1891(03)00051-x
更新日期：2003-10-01 00:00:00
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journal_title：Vascular pharmacology
pub_type： 杂志文章
doi：10.1016/j.vph.2016.05.015
更新日期：2016-09-01 00:00:00
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journal_title：Vascular pharmacology
pub_type： 杂志文章
doi：10.1016/j.vph.2020.106827
更新日期：2020-12-17 00:00:00
abstract：:We recently demonstrated that lipoic acid suppresses endotoxin-stimulated expression of inducible nitric oxide synthase and nitric oxide production in mouse macrophages. In this study, we tested whether lipoic acid suppresses these inflammatory mediators in the lungs of rats. Rats were assigned to receive either no sp...
journal_title：Vascular pharmacology
pub_type： 杂志文章
doi：10.1016/j.vph.2005.08.005
更新日期：2005-12-01 00:00:00
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journal_title：Vascular pharmacology
pub_type： 杂志文章
doi：10.1016/j.vph.2007.03.004
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journal_title：Vascular pharmacology
pub_type： 杂志文章,评审
doi：10.1016/j.vph.2016.02.002
更新日期：2016-07-01 00:00:00
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journal_title：Vascular pharmacology
pub_type： 杂志文章
doi：10.1016/s1537-1891(02)00338-5
更新日期：2003-02-01 00:00:00
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journal_title：Vascular pharmacology
pub_type： 杂志文章
doi：10.1016/j.vph.2016.11.009
更新日期：2017-01-01 00:00:00
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journal_title：Vascular pharmacology
pub_type： 杂志文章
doi：10.1016/j.vph.2015.08.011
更新日期：2016-04-01 00:00:00
abstract：:Unresolved endoplasmic reticulum (ER) stress, with the subsequent persistent activation of the unfolded protein response (UPR) is a well-recognized mechanism of endothelial cell apoptosis with a major impact on the integrity of the endothelium during the course of cardiovascular diseases. As in other cell types, Ca(2+...
journal_title：Vascular pharmacology
pub_type： 杂志文章
doi：10.1016/j.vph.2015.07.011
更新日期：2016-01-01 00:00:00
abstract：:The sulfur-containing amino acid, taurine, has been shown to ameliorate the vascular disorders. We examined the effects of taurine ingestion on intimal thickening following balloon injury. Balloon injury was induced in the left common carotid artery of Wistar rats. Taurine (3% (w/v)) was mixed in the drinking water fr...
journal_title：Vascular pharmacology
pub_type： 杂志文章
doi：10.1016/j.vph.2010.07.003
更新日期：2010-09-01 00:00:00
abstract：:Ion channels control electrical excitability in living cells. In mammalian heart, the opposing actions of Na(+) and Ca(2+) ion influx, and K(+) ion efflux, through cardiac ion channels determine the morphology and duration of action potentials in cardiac myocytes, thus controlling the heartbeat. The last decade has se...
journal_title：Vascular pharmacology
pub_type： 杂志文章,评审
doi：10.1016/j.vph.2005.07.013
更新日期：2006-02-01 00:00:00
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journal_title：Vascular pharmacology
pub_type： 杂志文章
doi：10.1016/j.vph.2005.11.006
更新日期：2006-04-01 00:00:00
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journal_title：Vascular pharmacology
pub_type： 杂志文章
doi：10.1016/j.vph.2008.01.009
更新日期：2008-04-01 00:00:00
abstract：:To investigate the vasorelaxant effect of fasudil mesylate (FM) in vivo and in vitro. The relaxation effect of FM was studied using cerebral vasospasm (CVS) model in vivo and isolated aortic rings in vitro. FM (0.35, 1.2, 3.5 mg·kg⁻¹) increased cerebrovascular flow (CVF) and femoral blood flow (FBF) dose-dependently i...
journal_title：Vascular pharmacology
pub_type： 杂志文章
doi：10.1016/j.vph.2011.06.005
更新日期：2011-11-01 00:00:00
abstract：:Angiostatin is an angiogenesis inhibitor in part generated by and released from platelets. Since platelets upon thrombus formation can give rise to areas of hypoxia, we investigated the effects of angiostatin on endothelial cell migration and apoptosis during hypoxia. Human microvascular endothelial cells (HMVEC-L) we...
journal_title：Vascular pharmacology
pub_type： 杂志文章
doi：10.1016/j.vph.2012.11.003
更新日期：2013-04-01 00:00:00
