NDLI: Advanced glycation end products impair $K_{Ca}3.1-$ and $K_{Ca}2.3-mediated$ vasodilatation via oxidative stress in rat mesenteric arteries

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Advanced glycation end products impair $K_{Ca}3.1-$ and $K_{Ca}2.3-mediated$ vasodilatation via oxidative stress in rat mesenteric arteries

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Zhao, Li-Mei Wang, Yan Ma, Xiao-Zhen Wang, Nan-Ping Deng, Xiu-Ling
Description	Country affiliation: China Author Affiliation: Zhao LM ( Department of Physiology and Pathophysiology, School of Medicine, Xi'an Jiaotong University, 76 West Yanta Road, Xi'an, 710061, Shaanxi, China.)
Abstract	The present study was designed to investigate the role of advanced glycation end products (AGEs) in intermediate-conductance and small-conductance $Ca^{2+}-activated$ potassium channels $(K_{Ca}3.1$ and $K_{Ca}2.3)-mediated$ relaxation in rat resistance arteries and the underlying mechanism. The endothelial function of mesenteric arteries was assessed with the use of wire myography. Expression levels of $K_{Ca}3.1$ and $K_{Ca}2.3$ were measured by using Western blot. Reactive oxygen species (ROS) were measured by using dihydroethidium and 2′, 7′-dichlorofluorescein diacetate. $K_{Ca}3.1$ and $K_{Ca}2.3-mediated$ vasodilatation responses to acetylcholine and NS309 (opener of $K_{Ca}3.1$ and $K_{Ca}2.3)$ were impaired by incubation of the third-order mesenteric arteries from normal rats with AGEs $(200 μg ml^{−1}$ for 3 h). In cultured human umbilical vein endothelial cells (HUVECs), AGEs increased ROS level and decreased the protein expression of $K_{Ca}3.1$ and $K_{Ca}2.3.$ Antioxidant alpha lipoic acid restored the impairment in both vasodilatation function and expression of $K_{Ca}3.1$ and $K_{Ca}2.3.$ $H_{2}O_{2}$ could mimic the effect of AGEs on the protein expression of $K_{Ca}3.1$ and $K_{Ca}2.3$ in cultured HUVECs. These results demonstrate for the first time that AGEs impaired $K_{Ca}3.1$ and $K_{Ca}2.3-mediated$ vasodilatation in rat mesenteric arteries via downregulation of both $K_{Ca}3.1$ and $K_{Ca}2.3,$ in which the enhanced oxidative stress was involved.
File Format	HTM / HTML
ISSN	00316768
Issue Number	2
Volume Number	466
e-ISSN	14322013
Journal	Pflügers Archiv - European Journal of Physiology
Language	English
Publisher	Springer
Publisher Date	2014-02-01
Publisher Place	Germany
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Discipline Physiology Glycosylation End Products, Advanced Pharmacology Intermediate-conductance Calcium-activated Potassium Channels Drug Effects Mesenteric Arteries Physiology Oxidative Stress Small-conductance Calcium-activated Potassium Channels Vasodilation Alkanes Animals Human Umbilical Vein Endothelial Cells Humans In Vitro Techniques Biosynthesis Male Ng-nitroarginine Methyl Ester Pyrazoles Quinolinium Compounds Rats Rats, Sprague-dawley Journal Article Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Physiology Physiology (medical) Clinical Biochemistry

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Advanced glycation end products impair KCa3.1- and KCa2.3-mediated vasodilatation via oxidative stress in rat mesenteric arteries

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