Abstract:
:The present study was designed to investigate the roles of enhanced arginase activity due to up-regulated arginases and the decreased hydroxyarginine for accelerating intimal hyperplasia with hyperglycemia. Thirteen weeks after injection of alloxan or physiological saline, endothelial denudation of the carotid artery was performed to induce intimal hyperplasia. The intimal hyperplasia occurred on 4 weeks following denudation was significantly accelerated by hyperglycemia. The method to measure L-arginine, endogenous NOS inhibitors such as monomethylarginine and asymmetric dimethylarginine, and hydroxyarginine as an intermediate of NO production simultaneously was established with the aid of high-performance liquid chromatography. In hyperglycemia group, the impaired cyclic GMP production as an indicator of NO production in endothelial cells was accompanied by the enhanced arginase activity together with increased expression of arginase I and II proteins, accumulated endogenous NOS inhibitors, reduced concentration of hydroxyarginine, and decreased DDAH activity in endothelial cells. However, NOS activity per se remained unchanged in the hyperglycemia group. Authentic hydroxyarginine inhibited arginase activity in a concentration-dependent manner. The inhibition of arginase with hydroxyarginine at a reduced concentration with hyperglycemia became significantly lower than that for the control. These results suggest that the accelerated intimal hyperplasia with hyperglycemia is closely related to the impaired NO production in endothelial cells, which results from accumulation of endogenous NOS inhibitors and accelerated arginase activity together with up-regulation of arginase I and II proteins. Decreased DDAH activity would bring about the accumulation of endogenous NOS inhibitors. Furthermore, reduced concentration of hydroxyarginine with hyperglycemia possibly results in an enhanced arginase activity in vivo, implicating partly in the impairment of NO production.
journal_name
Vascul Pharmacoljournal_title
Vascular pharmacologyauthors
Ishizaka M,Nagai A,Iwanaga M,Imamura M,Azuma Hdoi
10.1016/j.vph.2007.08.001subject
Has Abstractpub_date
2007-11-01 00:00:00pages
272-80issue
5-6eissn
1537-1891issn
1879-3649pii
S1537-1891(07)00122-Xjournal_volume
47pub_type
杂志文章abstract::Since the discovery of the importance of nitric oxide (NO) to the human body three decades ago, numerous laboratory and clinical studies have been done to explore its potential therapeutic actions on many organs. In the cardiovascular system, NO works as a volatile signaling molecule regulating the vascular permeabili...
journal_title:Vascular pharmacology
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journal_title:Vascular pharmacology
pub_type: 杂志文章,评审
doi:10.1016/j.vph.2006.11.005
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journal_title:Vascular pharmacology
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更新日期:2013-03-01 00:00:00
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journal_title:Vascular pharmacology
pub_type: 杂志文章,评审
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journal_title:Vascular pharmacology
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更新日期:2020-01-01 00:00:00
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journal_title:Vascular pharmacology
pub_type: 杂志文章
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journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2020.106821
更新日期:2021-02-01 00:00:00
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journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2019.01.005
更新日期:2019-04-01 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,评审
doi:10.1016/j.vph.2014.10.006
更新日期:2014-12-01 00:00:00
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journal_title:Vascular pharmacology
pub_type: 杂志文章,评审
doi:10.1016/j.vph.2005.01.009
更新日期:2005-02-01 00:00:00
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journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2011.03.001
更新日期:2011-07-01 00:00:00
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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
pub_type: 杂志文章
doi:10.1016/j.vph.2008.09.001
更新日期:2009-01-01 00:00:00
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journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2016.05.007
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/j.vph.2020.106822
更新日期:2020-11-21 00:00:00
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journal_title:Vascular pharmacology
pub_type: 杂志文章,评审
doi:10.1016/j.vph.2005.11.014
更新日期:2006-07-01 00:00:00
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journal_title:Vascular pharmacology
pub_type: 杂志文章,评审
doi:10.1016/j.vph.2016.05.016
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journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2004.10.002
更新日期:2004-05-01 00:00:00
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journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2012.11.004
更新日期:2013-04-01 00:00:00
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journal_title:Vascular pharmacology
pub_type: 杂志文章,评审
doi:10.1016/j.vph.2017.11.006
更新日期:2018-02-01 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
abstract::We investigated the regulation of the epithelial sodium channel (ENaC) in human bone marrow endothelial cells (HBMEC) responding to mineralocorticoid hormones and other accessory effectors. The message for both the mineralocorticoid receptor (MCR) and the alpha subunit of ENaC was expressed in HBMEC as predicted bands...
journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2003.08.003
更新日期:2004-01-01 00:00:00
abstract::Cardiovascular diseases are the major challenge to modern medicine. Intervention to cardiovascular cells is crucial for treatment of the diseases. Here we report a novel intervention to vascular smooth muscle (VSM) cells by optogenetics. Channelrhodopsin in a tandem with YFP was selectively expressed in smooth muscle ...
journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2015.03.006
更新日期:2015-08-01 00:00:00
abstract::The early stages of invasion are characterized by the extracellular proteolysis and the accumulation of specialized extracellular matrix (ECM) scaffold, that are responsible for the development of vascular bed, endothelial cell proliferation and invasion of tumour cells. The ground substance of provisional matrix cons...
journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2006.12.004
更新日期:2007-06-01 00:00:00
abstract::Endothelial cell dysfunction may play an important role in the development of various vascular diseases, including atherosclerosis. Here we investigated whether lithium chloride (LiCl), an inhibitor of glycogen synthase kinase-3β (GSK-3β), could counteract atherosclerosis induced by a high-fat diet in ApoE⁻/⁻ mice. Te...
journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2010.09.004
更新日期:2010-11-01 00:00:00
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journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2006.06.008
更新日期:2006-12-01 00:00:00
abstract::Norepinephrine (NE) responses are larger in renal and femoral veins compared to phenylephrine (PE). These differences may be due to the subtypes of adrenoceptor involved in these responses or to the involvement of local modulatory mechanisms. Therefore, the present study investigated in organ bath the adrenoceptor sub...
journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2015.06.017
更新日期:2015-09-01 00:00:00
abstract:BACKGROUND:Macrophages play a central role in atherosclerosis development and progression, hence, targeting macrophage activity is considered an attractive therapeutic. Recently, we documented nanomedicinal delivery of the anti-inflammatory compound prednisolone to atherosclerotic plaque macrophages in patients, which ...
journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2016.04.006
更新日期:2016-07-01 00:00:00