Effects of allitridum on the transient outward potassium current in rats with heart failure

Effects of allitridum on the transient outward potassium current in rats with heart failure

Objective To study the effect of allitridum on the transient outward potassium current （Ito） of ventricular myocytes in heart failure （HF）. Methods The dual enzymatic method was used to separate single ventricular myocytes from Sprague Dawley rats. Patch-clamping was used to record Ito and analyze t...

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Veröffentlicht in:Journal of geriatric cardiology : JGC 2016-09, Vol.13 (9), p.783-788
Hauptverfasser: Zhao, Xiao-Jing, Lin, Kun, Zhang, Yu, Xu, Bin, Liu, Li, Fu, Yi-Cheng, Chen, Xi, Cai, Zhong-Qi, Wu, Zhi-Juan, Huang, Yun, Li, Yang
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container_issue 9
container_start_page 783
container_title Journal of geriatric cardiology : JGC
container_volume 13
creator Zhao, Xiao-Jing
Lin, Kun
Zhang, Yu
Xu, Bin
Liu, Li
Fu, Yi-Cheng
Chen, Xi
Cai, Zhong-Qi
Wu, Zhi-Juan
Huang, Yun
Li, Yang
description Objective To study the effect of allitridum on the transient outward potassium current （Ito） of ventricular myocytes in heart failure （HF）. Methods The dual enzymatic method was used to separate single ventricular myocytes from Sprague Dawley rats. Patch-clamping was used to record Ito and analyze the effect of allitridum on the current. Results The Ito current had a significant decrease in the HF group, compared with the control group. The density of Ito in the HF group was increased after treatment of allitridum （30 μmol/L）. The peak current densities of Ito were enhanced in the HF group from 6.01 ±0.30 pA/pF to 8.41 ±0.54 pA/pF （P 〈 0.01） at ＋50 mV after treatment with allitridum （30 μmol/L）. We also determined the effect of allitridum on the gating mechanism of the Ito in the HF group. Conclusions We found that allitridum increased the Ito by accelerating the activation of channels and shortened the time constants of inactivation, and allitridum decreased the remodeling of Ito in ventricular myocytes of rats with HF.
doi_str_mv 10.11909/j.issn.1671-5411.2016.09.005
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Methods The dual enzymatic method was used to separate single ventricular myocytes from Sprague Dawley rats. Patch-clamping was used to record Ito and analyze the effect of allitridum on the current. Results The Ito current had a significant decrease in the HF group, compared with the control group. The density of Ito in the HF group was increased after treatment of allitridum （30 μmol/L）. The peak current densities of Ito were enhanced in the HF group from 6.01 ±0.30 pA/pF to 8.41 ±0.54 pA/pF （P 〈 0.01） at ＋50 mV after treatment with allitridum （30 μmol/L）. We also determined the effect of allitridum on the gating mechanism of the Ito in the HF group. Conclusions We found that allitridum increased the Ito by accelerating the activation of channels and shortened the time constants of inactivation, and allitridum decreased the remodeling of Ito in ventricular myocytes of rats with HF.</description><identifier>ISSN: 1671-5411</identifier><identifier>DOI: 10.11909/j.issn.1671-5411.2016.09.005</identifier><identifier>PMID: 27899943</identifier><language>eng</language><publisher>China: Science Press</publisher><ispartof>Journal of geriatric cardiology : JGC, 2016-09, Vol.13 (9), p.783-788</ispartof><rights>Institute of Geriatric Cardiology 2016</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Uhttp://image.cqvip.com/vip1000/qk/88644X/88644X.jpg</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5122504/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5122504/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27899943$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhao, Xiao-Jing</creatorcontrib><creatorcontrib>Lin, Kun</creatorcontrib><creatorcontrib>Zhang, Yu</creatorcontrib><creatorcontrib>Xu, Bin</creatorcontrib><creatorcontrib>Liu, Li</creatorcontrib><creatorcontrib>Fu, Yi-Cheng</creatorcontrib><creatorcontrib>Chen, Xi</creatorcontrib><creatorcontrib>Cai, Zhong-Qi</creatorcontrib><creatorcontrib>Wu, Zhi-Juan</creatorcontrib><creatorcontrib>Huang, Yun</creatorcontrib><creatorcontrib>Li, Yang</creatorcontrib><title>Effects of allitridum on the transient outward potassium current in rats with heart failure</title><title>Journal of geriatric cardiology : JGC</title><addtitle>Journal of Geriatric Cardiology</addtitle><description>Objective To study the effect of allitridum on the transient outward potassium current （Ito） of ventricular myocytes in heart failure （HF）. Methods The dual enzymatic method was used to separate single ventricular myocytes from Sprague Dawley rats. Patch-clamping was used to record Ito and analyze the effect of allitridum on the current. Results The Ito current had a significant decrease in the HF group, compared with the control group. The density of Ito in the HF group was increased after treatment of allitridum （30 μmol/L）. The peak current densities of Ito were enhanced in the HF group from 6.01 ±0.30 pA/pF to 8.41 ±0.54 pA/pF （P 〈 0.01） at ＋50 mV after treatment with allitridum （30 μmol/L）. We also determined the effect of allitridum on the gating mechanism of the Ito in the HF group. 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Methods The dual enzymatic method was used to separate single ventricular myocytes from Sprague Dawley rats. Patch-clamping was used to record Ito and analyze the effect of allitridum on the current. Results The Ito current had a significant decrease in the HF group, compared with the control group. The density of Ito in the HF group was increased after treatment of allitridum （30 μmol/L）. The peak current densities of Ito were enhanced in the HF group from 6.01 ±0.30 pA/pF to 8.41 ±0.54 pA/pF （P 〈 0.01） at ＋50 mV after treatment with allitridum （30 μmol/L）. We also determined the effect of allitridum on the gating mechanism of the Ito in the HF group. Conclusions We found that allitridum increased the Ito by accelerating the activation of channels and shortened the time constants of inactivation, and allitridum decreased the remodeling of Ito in ventricular myocytes of rats with HF.</abstract><cop>China</cop><pub>Science Press</pub><pmid>27899943</pmid><doi>10.11909/j.issn.1671-5411.2016.09.005</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record>
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title Effects of allitridum on the transient outward potassium current in rats with heart failure
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