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Bradykinin induces vascular contraction after hemorrhagic shock in rats

Abstract Background Bradykinin (BK) has many biological effects in inflammation, allergy, and septic shock. Studies have shown that low doses of BK can induce vascular relaxation and high doses can induce vascular contraction in many pathophysiological conditions, but the role and mechanisms that hi...

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Published in:	The Journal of surgical research 2015, Vol.193 (1), p.334-343
Main Authors:	Zhang, Jie, MD, Yang, Guang-ming, MD, Zhu, Yu, MS, Peng, Xiao-yong, MS, Liu, Liang-ming, MD, Li, Tao, MD
Format:	Article
Language:	English
Subjects:	Animals Bradykinin Bradykinin - pharmacology Connexin Connexin 43 - genetics Dose-Response Relationship, Drug Hypoxia - drug therapy Mesenteric Artery, Superior - drug effects Oligonucleotides, Antisense - pharmacology PKC Protein Kinase C-alpha - metabolism Protein Kinase C-epsilon - metabolism rac1 GTP-Binding Protein - metabolism Rats, Sprague-Dawley rho-Associated Kinases - metabolism Shock Shock, Hemorrhagic - drug therapy Shock, Hemorrhagic - metabolism Signal Transduction - drug effects Surgery Vascular reactivity Vasoconstriction - drug effects Vasoconstrictor Agents - pharmacology
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creator	Zhang, Jie, MD Yang, Guang-ming, MD Zhu, Yu, MS Peng, Xiao-yong, MS Liu, Liang-ming, MD Li, Tao, MD
description	Abstract Background Bradykinin (BK) has many biological effects in inflammation, allergy, and septic shock. Studies have shown that low doses of BK can induce vascular relaxation and high doses can induce vascular contraction in many pathophysiological conditions, but the role and mechanisms that high doses of BK have on vascular contraction in hemorrhagic shock are not clear. Methods With hemorrhagic-shock rats and hypoxia-treated superior mesenteric artery (SMA), we investigated the role and mechanisms of high doses of BK-induced vascular contraction in hemorrhagic shock. Results High doses of BK (500–50,000 ng/kg in vivo or 10−10 to 10−5 mol/L in vitro ) dose dependently induced vascular contraction of SMA and increased the vascular calcium sensitivity in normal and hemorrhagic-shock rats. Less than 10−10 mol/L of BK induced vascular dilation BK-induced increase of vascular contractile response and calcium sensitivity was reduced by denudation of the endothelium, 18α-glycyrrhetic acid (an inhibitor of myoendothelial gap junction) and connexin 43 antisense oligodeoxynucleotide. Further studies found that high concentrations of BK-induced vascular contraction in hemorrhagic shock was closely related to the activation of Rho A–Rho kinase pathway and Protein Kinase C (PKC) α and ε. Conclusions High doses of BK can induce vascular contraction in hemorrhagic shock condition, which is endothelium and myoendothelial gap junction dependent. Cx43-mediated activation of Rho A–Rho kinase and Protein Kinase C (PKC) pathway plays a very important role in this process. This finding provided a new angle of view to the biological role of BK in other pathophysiological conditions such as hemorrhagic shock or hypoxia.
doi_str_mv	10.1016/j.jss.2014.06.033
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Studies have shown that low doses of BK can induce vascular relaxation and high doses can induce vascular contraction in many pathophysiological conditions, but the role and mechanisms that high doses of BK have on vascular contraction in hemorrhagic shock are not clear. Methods With hemorrhagic-shock rats and hypoxia-treated superior mesenteric artery (SMA), we investigated the role and mechanisms of high doses of BK-induced vascular contraction in hemorrhagic shock. Results High doses of BK (500–50,000 ng/kg in vivo or 10−10 to 10−5 mol/L in vitro ) dose dependently induced vascular contraction of SMA and increased the vascular calcium sensitivity in normal and hemorrhagic-shock rats. Less than 10−10 mol/L of BK induced vascular dilation BK-induced increase of vascular contractile response and calcium sensitivity was reduced by denudation of the endothelium, 18α-glycyrrhetic acid (an inhibitor of myoendothelial gap junction) and connexin 43 antisense oligodeoxynucleotide. Further studies found that high concentrations of BK-induced vascular contraction in hemorrhagic shock was closely related to the activation of Rho A–Rho kinase pathway and Protein Kinase C (PKC) α and ε. Conclusions High doses of BK can induce vascular contraction in hemorrhagic shock condition, which is endothelium and myoendothelial gap junction dependent. Cx43-mediated activation of Rho A–Rho kinase and Protein Kinase C (PKC) pathway plays a very important role in this process. This finding provided a new angle of view to the biological role of BK in other pathophysiological conditions such as hemorrhagic shock or hypoxia.</description><identifier>ISSN: 0022-4804</identifier><identifier>EISSN: 1095-8673</identifier><identifier>DOI: 10.1016/j.jss.2014.06.033</identifier><identifier>PMID: 25048290</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Animals ; Bradykinin ; Bradykinin - pharmacology ; Connexin ; Connexin 43 - genetics ; Dose-Response Relationship, Drug ; Hypoxia - drug therapy ; Mesenteric Artery, Superior - drug effects ; Oligonucleotides, Antisense - pharmacology ; PKC ; Protein Kinase C-alpha - metabolism ; Protein Kinase C-epsilon - metabolism ; rac1 GTP-Binding Protein - metabolism ; Rats, Sprague-Dawley ; rho-Associated Kinases - metabolism ; Shock ; Shock, Hemorrhagic - drug therapy ; Shock, Hemorrhagic - metabolism ; Signal Transduction - drug effects ; Surgery ; Vascular reactivity ; Vasoconstriction - drug effects ; Vasoconstrictor Agents - pharmacology</subject><ispartof>The Journal of surgical research, 2015, Vol.193 (1), p.334-343</ispartof><rights>Elsevier Inc.</rights><rights>2015 Elsevier Inc.</rights><rights>Copyright © 2015 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c408t-bcf51a298c708bdff8599cab88fee488a0dea68a5b869231920b64f9e47ec7213</citedby><cites>FETCH-LOGICAL-c408t-bcf51a298c708bdff8599cab88fee488a0dea68a5b869231920b64f9e47ec7213</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,786,790,4043,27956,27957,27958</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25048290$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhang, Jie, MD</creatorcontrib><creatorcontrib>Yang, Guang-ming, MD</creatorcontrib><creatorcontrib>Zhu, Yu, MS</creatorcontrib><creatorcontrib>Peng, Xiao-yong, MS</creatorcontrib><creatorcontrib>Liu, Liang-ming, MD</creatorcontrib><creatorcontrib>Li, Tao, MD</creatorcontrib><title>Bradykinin induces vascular contraction after hemorrhagic shock in rats</title><title>The Journal of surgical research</title><addtitle>J Surg Res</addtitle><description>Abstract Background Bradykinin (BK) has many biological effects in inflammation, allergy, and septic shock. Studies have shown that low doses of BK can induce vascular relaxation and high doses can induce vascular contraction in many pathophysiological conditions, but the role and mechanisms that high doses of BK have on vascular contraction in hemorrhagic shock are not clear. Methods With hemorrhagic-shock rats and hypoxia-treated superior mesenteric artery (SMA), we investigated the role and mechanisms of high doses of BK-induced vascular contraction in hemorrhagic shock. Results High doses of BK (500–50,000 ng/kg in vivo or 10−10 to 10−5 mol/L in vitro ) dose dependently induced vascular contraction of SMA and increased the vascular calcium sensitivity in normal and hemorrhagic-shock rats. Less than 10−10 mol/L of BK induced vascular dilation BK-induced increase of vascular contractile response and calcium sensitivity was reduced by denudation of the endothelium, 18α-glycyrrhetic acid (an inhibitor of myoendothelial gap junction) and connexin 43 antisense oligodeoxynucleotide. Further studies found that high concentrations of BK-induced vascular contraction in hemorrhagic shock was closely related to the activation of Rho A–Rho kinase pathway and Protein Kinase C (PKC) α and ε. Conclusions High doses of BK can induce vascular contraction in hemorrhagic shock condition, which is endothelium and myoendothelial gap junction dependent. Cx43-mediated activation of Rho A–Rho kinase and Protein Kinase C (PKC) pathway plays a very important role in this process. This finding provided a new angle of view to the biological role of BK in other pathophysiological conditions such as hemorrhagic shock or hypoxia.</description><subject>Animals</subject><subject>Bradykinin</subject><subject>Bradykinin - pharmacology</subject><subject>Connexin</subject><subject>Connexin 43 - genetics</subject><subject>Dose-Response Relationship, Drug</subject><subject>Hypoxia - drug therapy</subject><subject>Mesenteric Artery, Superior - drug effects</subject><subject>Oligonucleotides, Antisense - pharmacology</subject><subject>PKC</subject><subject>Protein Kinase C-alpha - metabolism</subject><subject>Protein Kinase C-epsilon - metabolism</subject><subject>rac1 GTP-Binding Protein - metabolism</subject><subject>Rats, Sprague-Dawley</subject><subject>rho-Associated Kinases - metabolism</subject><subject>Shock</subject><subject>Shock, Hemorrhagic - drug therapy</subject><subject>Shock, Hemorrhagic - metabolism</subject><subject>Signal Transduction - drug effects</subject><subject>Surgery</subject><subject>Vascular reactivity</subject><subject>Vasoconstriction - drug effects</subject><subject>Vasoconstrictor Agents - pharmacology</subject><issn>0022-4804</issn><issn>1095-8673</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><recordid>eNp9kcFu1DAQhi0EotvCA3BBOXJJGDuOYwsJCSraIlXqoXC2nMmEdTYbFzuptG-PV9ty4MBpNNL3_9J8w9g7DhUHrj6O1ZhSJYDLClQFdf2CbTiYptSqrV-yDYAQpdQgz9h5SiPk3bT1a3YmGpBaGNiw66_R9Yedn_1c-LlfkVLx6BKuk4sFhnmJDhcf5sINC8ViS_sQ49b98likbcBdDhXRLekNezW4KdHbp3nBfl59-3F5U97eXX-__HJbogS9lB0ODXfCaGxBd_0w6MYYdJ3WA5HU2kFPTmnXdFoZUXMjoFNyMCRbwlbw-oJ9OPU-xPB7pbTYvU9I0-RmCmuyXNVtoyRvZUb5CcUYUoo02Ifo9y4eLAd79GdHm_3Zoz8LymZ_OfP-qX7t9tT_TTwLy8CnE0D5yEdP0Sb0NCP1PhIutg_-v_Wf_0njlNWjm3Z0oDSGNc7ZnuU2CQv2_vjA4_-4BGi0kPUfbtaV8g</recordid><startdate>2015</startdate><enddate>2015</enddate><creator>Zhang, Jie, MD</creator><creator>Yang, Guang-ming, MD</creator><creator>Zhu, Yu, MS</creator><creator>Peng, Xiao-yong, MS</creator><creator>Liu, Liang-ming, MD</creator><creator>Li, Tao, MD</creator><general>Elsevier Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>2015</creationdate><title>Bradykinin induces vascular contraction after hemorrhagic shock in rats</title><author>Zhang, Jie, MD ; Yang, Guang-ming, MD ; Zhu, Yu, MS ; Peng, Xiao-yong, MS ; Liu, Liang-ming, MD ; Li, Tao, MD</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c408t-bcf51a298c708bdff8599cab88fee488a0dea68a5b869231920b64f9e47ec7213</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Animals</topic><topic>Bradykinin</topic><topic>Bradykinin - pharmacology</topic><topic>Connexin</topic><topic>Connexin 43 - genetics</topic><topic>Dose-Response Relationship, Drug</topic><topic>Hypoxia - drug therapy</topic><topic>Mesenteric Artery, Superior - drug effects</topic><topic>Oligonucleotides, Antisense - pharmacology</topic><topic>PKC</topic><topic>Protein Kinase C-alpha - metabolism</topic><topic>Protein Kinase C-epsilon - metabolism</topic><topic>rac1 GTP-Binding Protein - metabolism</topic><topic>Rats, Sprague-Dawley</topic><topic>rho-Associated Kinases - metabolism</topic><topic>Shock</topic><topic>Shock, Hemorrhagic - drug therapy</topic><topic>Shock, Hemorrhagic - metabolism</topic><topic>Signal Transduction - drug effects</topic><topic>Surgery</topic><topic>Vascular reactivity</topic><topic>Vasoconstriction - drug effects</topic><topic>Vasoconstrictor Agents - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhang, Jie, MD</creatorcontrib><creatorcontrib>Yang, Guang-ming, MD</creatorcontrib><creatorcontrib>Zhu, Yu, MS</creatorcontrib><creatorcontrib>Peng, Xiao-yong, MS</creatorcontrib><creatorcontrib>Liu, Liang-ming, MD</creatorcontrib><creatorcontrib>Li, Tao, MD</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>The Journal of surgical research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhang, Jie, MD</au><au>Yang, Guang-ming, MD</au><au>Zhu, Yu, MS</au><au>Peng, Xiao-yong, MS</au><au>Liu, Liang-ming, MD</au><au>Li, Tao, MD</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Bradykinin induces vascular contraction after hemorrhagic shock in rats</atitle><jtitle>The Journal of surgical research</jtitle><addtitle>J Surg Res</addtitle><date>2015</date><risdate>2015</risdate><volume>193</volume><issue>1</issue><spage>334</spage><epage>343</epage><pages>334-343</pages><issn>0022-4804</issn><eissn>1095-8673</eissn><notes>ObjectType-Article-1</notes><notes>SourceType-Scholarly Journals-1</notes><notes>ObjectType-Feature-2</notes><notes>content type line 23</notes><abstract>Abstract Background Bradykinin (BK) has many biological effects in inflammation, allergy, and septic shock. Studies have shown that low doses of BK can induce vascular relaxation and high doses can induce vascular contraction in many pathophysiological conditions, but the role and mechanisms that high doses of BK have on vascular contraction in hemorrhagic shock are not clear. Methods With hemorrhagic-shock rats and hypoxia-treated superior mesenteric artery (SMA), we investigated the role and mechanisms of high doses of BK-induced vascular contraction in hemorrhagic shock. Results High doses of BK (500–50,000 ng/kg in vivo or 10−10 to 10−5 mol/L in vitro ) dose dependently induced vascular contraction of SMA and increased the vascular calcium sensitivity in normal and hemorrhagic-shock rats. Less than 10−10 mol/L of BK induced vascular dilation BK-induced increase of vascular contractile response and calcium sensitivity was reduced by denudation of the endothelium, 18α-glycyrrhetic acid (an inhibitor of myoendothelial gap junction) and connexin 43 antisense oligodeoxynucleotide. Further studies found that high concentrations of BK-induced vascular contraction in hemorrhagic shock was closely related to the activation of Rho A–Rho kinase pathway and Protein Kinase C (PKC) α and ε. Conclusions High doses of BK can induce vascular contraction in hemorrhagic shock condition, which is endothelium and myoendothelial gap junction dependent. Cx43-mediated activation of Rho A–Rho kinase and Protein Kinase C (PKC) pathway plays a very important role in this process. This finding provided a new angle of view to the biological role of BK in other pathophysiological conditions such as hemorrhagic shock or hypoxia.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>25048290</pmid><doi>10.1016/j.jss.2014.06.033</doi><tpages>10</tpages></addata></record>
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subjects	Animals Bradykinin Bradykinin - pharmacology Connexin Connexin 43 - genetics Dose-Response Relationship, Drug Hypoxia - drug therapy Mesenteric Artery, Superior - drug effects Oligonucleotides, Antisense - pharmacology PKC Protein Kinase C-alpha - metabolism Protein Kinase C-epsilon - metabolism rac1 GTP-Binding Protein - metabolism Rats, Sprague-Dawley rho-Associated Kinases - metabolism Shock Shock, Hemorrhagic - drug therapy Shock, Hemorrhagic - metabolism Signal Transduction - drug effects Surgery Vascular reactivity Vasoconstriction - drug effects Vasoconstrictor Agents - pharmacology
title	Bradykinin induces vascular contraction after hemorrhagic shock in rats
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