Baroreflex deficiency hampers angiogenesis after myocardial infarction via acetylcholine-α7-nicotinic ACh receptor in rats
Angiogenesis is critical for re-establishing blood supply to ischaemic myocardium after myocardial infarction (MI). Human studies have associated arterial baroreflex (ABR) deficiency with higher rate of sudden death after MI. The present work was designed to examine whether ABR deficiency affects an...
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| Veröffentlicht in: | European heart journal 2013-08, Vol.34 (30), p.2412-2420 |
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| container_title | European heart journal |
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| creator | Yu, Jian-Guang Song, Shu-Wei Shu, He Fan, Sai-Jun Liu, Ai-Jun Liu, Chong Guo, Wei Guo, Jin-Min Miao, Chao-Yu Su, Ding-Feng |
| description | Angiogenesis is critical for re-establishing blood supply to ischaemic myocardium after myocardial infarction (MI). Human studies have associated arterial baroreflex (ABR) deficiency with higher rate of sudden death after MI. The present work was designed to examine whether ABR deficiency affects angiogenesis in MI rats.
Baroreflex sensitivity (BRS) was determined in conscious rats at 1 month after occlusion of the left anterior descending coronary artery. The survival time was significantly shorter in Sprague-Dawley rats with BRS |
| doi_str_mv | 10.1093/eurheartj/ehr299 |
| format | Article |
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Baroreflex sensitivity (BRS) was determined in conscious rats at 1 month after occlusion of the left anterior descending coronary artery. The survival time was significantly shorter in Sprague-Dawley rats with BRS <0.60 ms/mmHg vs. those with BRS ≥0.60 ms/mmHg. Sinoaortic denervation destroyed ABR, and decreased capillary density, regional blood flow and vascular endothelial growth factor (VEGF) concentration after MI. Ketanserin (0.6 mg/kg/day) enhanced BRS, and increased capillary density, regional blood flow, and VEGF. Sinoaortic denervation also reduced the expression of vesicular acetylcholine (ACh) transporter and α7-nicotinic ACh receptor (α7-nAChR). Angiogenesis after MI was significantly attenuated in α7-nAChR knockout mice. In contrast, increase in endogenous ACh with cholinesterase inhibitor pyridostigmine (30 mg/kg/day) increased angiogenesis after MI. In cultured cardiac microvascular endothelial cells, ACh stimulated the expression of VEGF, phosphorylation of VEGF receptor 2, and tube formation in a manner dependent upon α7-nAChR.
Our results demonstrated that ABR deficiency could attenuate angiogenesis in ischaemic myocardium. These findings provide further mechanistic basis for enhancing baroreflex function in the treatment of MI.</description><identifier>EISSN: 1522-9645</identifier><identifier>DOI: 10.1093/eurheartj/ehr299</identifier><identifier>PMID: 21849351</identifier><language>eng</language><publisher>England</publisher><subject>Acetylcholine - pharmacology ; Acetylcholine - physiology ; alpha7 Nicotinic Acetylcholine Receptor - metabolism ; alpha7 Nicotinic Acetylcholine Receptor - physiology ; Angiogenesis Inducing Agents - pharmacology ; Animals ; Baroreflex - physiology ; Blood Pressure - physiology ; Capillaries - physiology ; Cholinergic Agonists - pharmacology ; Cholinesterase Inhibitors - pharmacology ; Coronary Vessels - physiology ; Denervation - methods ; Ketanserin - pharmacology ; Mice ; Mice, Knockout ; Myocardial Infarction - physiopathology ; Neovascularization, Physiologic - physiology ; Pyridostigmine Bromide - pharmacology ; Rats ; Rats, Sprague-Dawley</subject><ispartof>European heart journal, 2013-08, Vol.34 (30), p.2412-2420</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21849351$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yu, Jian-Guang</creatorcontrib><creatorcontrib>Song, Shu-Wei</creatorcontrib><creatorcontrib>Shu, He</creatorcontrib><creatorcontrib>Fan, Sai-Jun</creatorcontrib><creatorcontrib>Liu, Ai-Jun</creatorcontrib><creatorcontrib>Liu, Chong</creatorcontrib><creatorcontrib>Guo, Wei</creatorcontrib><creatorcontrib>Guo, Jin-Min</creatorcontrib><creatorcontrib>Miao, Chao-Yu</creatorcontrib><creatorcontrib>Su, Ding-Feng</creatorcontrib><title>Baroreflex deficiency hampers angiogenesis after myocardial infarction via acetylcholine-α7-nicotinic ACh receptor in rats</title><title>European heart journal</title><addtitle>Eur Heart J</addtitle><description>Angiogenesis is critical for re-establishing blood supply to ischaemic myocardium after myocardial infarction (MI). Human studies have associated arterial baroreflex (ABR) deficiency with higher rate of sudden death after MI. The present work was designed to examine whether ABR deficiency affects angiogenesis in MI rats.
Baroreflex sensitivity (BRS) was determined in conscious rats at 1 month after occlusion of the left anterior descending coronary artery. The survival time was significantly shorter in Sprague-Dawley rats with BRS <0.60 ms/mmHg vs. those with BRS ≥0.60 ms/mmHg. Sinoaortic denervation destroyed ABR, and decreased capillary density, regional blood flow and vascular endothelial growth factor (VEGF) concentration after MI. Ketanserin (0.6 mg/kg/day) enhanced BRS, and increased capillary density, regional blood flow, and VEGF. Sinoaortic denervation also reduced the expression of vesicular acetylcholine (ACh) transporter and α7-nicotinic ACh receptor (α7-nAChR). Angiogenesis after MI was significantly attenuated in α7-nAChR knockout mice. In contrast, increase in endogenous ACh with cholinesterase inhibitor pyridostigmine (30 mg/kg/day) increased angiogenesis after MI. In cultured cardiac microvascular endothelial cells, ACh stimulated the expression of VEGF, phosphorylation of VEGF receptor 2, and tube formation in a manner dependent upon α7-nAChR.
Our results demonstrated that ABR deficiency could attenuate angiogenesis in ischaemic myocardium. These findings provide further mechanistic basis for enhancing baroreflex function in the treatment of MI.</description><subject>Acetylcholine - pharmacology</subject><subject>Acetylcholine - physiology</subject><subject>alpha7 Nicotinic Acetylcholine Receptor - metabolism</subject><subject>alpha7 Nicotinic Acetylcholine Receptor - physiology</subject><subject>Angiogenesis Inducing Agents - pharmacology</subject><subject>Animals</subject><subject>Baroreflex - physiology</subject><subject>Blood Pressure - physiology</subject><subject>Capillaries - physiology</subject><subject>Cholinergic Agonists - pharmacology</subject><subject>Cholinesterase Inhibitors - pharmacology</subject><subject>Coronary Vessels - physiology</subject><subject>Denervation - methods</subject><subject>Ketanserin - pharmacology</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>Myocardial Infarction - physiopathology</subject><subject>Neovascularization, Physiologic - physiology</subject><subject>Pyridostigmine Bromide - pharmacology</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><issn>1522-9645</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo1kL1OwzAcxC0kREthZ0IeWULjryQeS8WXVIkF5six_2lcJXGwHUTEU_EiPBORKMudTvrdDYfQFUlvSSrZGkbfgPLxsIbGUylP0JIIShOZcbFA5yEc0jQtMpKdoQUlBZdMkCX6ulPeeahb-MQGaqst9HrCjeoG8AGrfm_dHnoIdg51BI-7yWnljVUttn2tvI7W9fjDKqw0xKnVjWttD8nPd570VrtoZ8WbbYM9aBii83MPexXDBTqtVRvg8ugr9PZw_7p9SnYvj8_bzS4ZCM1iAjVnAkwlikqQihpORZ4LqJgGVmdCc6lEZYzkRDOaVobyAnie14TS3BDG2Qrd_O0O3r2PEGLZ2aChbVUPbgwl4UQyTkkuZ_T6iI5VB6YcvO2Un8r_w9gvMi5w3A</recordid><startdate>201308</startdate><enddate>201308</enddate><creator>Yu, Jian-Guang</creator><creator>Song, Shu-Wei</creator><creator>Shu, He</creator><creator>Fan, Sai-Jun</creator><creator>Liu, Ai-Jun</creator><creator>Liu, Chong</creator><creator>Guo, Wei</creator><creator>Guo, Jin-Min</creator><creator>Miao, Chao-Yu</creator><creator>Su, Ding-Feng</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope></search><sort><creationdate>201308</creationdate><title>Baroreflex deficiency hampers angiogenesis after myocardial infarction via acetylcholine-α7-nicotinic ACh receptor in rats</title><author>Yu, Jian-Guang ; Song, Shu-Wei ; Shu, He ; Fan, Sai-Jun ; Liu, Ai-Jun ; Liu, Chong ; Guo, Wei ; Guo, Jin-Min ; Miao, Chao-Yu ; Su, Ding-Feng</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p126t-ef435edb58b51b2d425775eb3ce3f65c49a5bdd941c320bd248e477f1227d1343</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Acetylcholine - pharmacology</topic><topic>Acetylcholine - physiology</topic><topic>alpha7 Nicotinic Acetylcholine Receptor - metabolism</topic><topic>alpha7 Nicotinic Acetylcholine Receptor - physiology</topic><topic>Angiogenesis Inducing Agents - pharmacology</topic><topic>Animals</topic><topic>Baroreflex - physiology</topic><topic>Blood Pressure - physiology</topic><topic>Capillaries - physiology</topic><topic>Cholinergic Agonists - pharmacology</topic><topic>Cholinesterase Inhibitors - pharmacology</topic><topic>Coronary Vessels - physiology</topic><topic>Denervation - methods</topic><topic>Ketanserin - pharmacology</topic><topic>Mice</topic><topic>Mice, Knockout</topic><topic>Myocardial Infarction - physiopathology</topic><topic>Neovascularization, Physiologic - physiology</topic><topic>Pyridostigmine Bromide - pharmacology</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yu, Jian-Guang</creatorcontrib><creatorcontrib>Song, Shu-Wei</creatorcontrib><creatorcontrib>Shu, He</creatorcontrib><creatorcontrib>Fan, Sai-Jun</creatorcontrib><creatorcontrib>Liu, Ai-Jun</creatorcontrib><creatorcontrib>Liu, Chong</creatorcontrib><creatorcontrib>Guo, Wei</creatorcontrib><creatorcontrib>Guo, Jin-Min</creatorcontrib><creatorcontrib>Miao, Chao-Yu</creatorcontrib><creatorcontrib>Su, Ding-Feng</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><jtitle>European heart journal</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yu, Jian-Guang</au><au>Song, Shu-Wei</au><au>Shu, He</au><au>Fan, Sai-Jun</au><au>Liu, Ai-Jun</au><au>Liu, Chong</au><au>Guo, Wei</au><au>Guo, Jin-Min</au><au>Miao, Chao-Yu</au><au>Su, Ding-Feng</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Baroreflex deficiency hampers angiogenesis after myocardial infarction via acetylcholine-α7-nicotinic ACh receptor in rats</atitle><jtitle>European heart journal</jtitle><addtitle>Eur Heart J</addtitle><date>2013-08</date><risdate>2013</risdate><volume>34</volume><issue>30</issue><spage>2412</spage><epage>2420</epage><pages>2412-2420</pages><eissn>1522-9645</eissn><abstract>Angiogenesis is critical for re-establishing blood supply to ischaemic myocardium after myocardial infarction (MI). Human studies have associated arterial baroreflex (ABR) deficiency with higher rate of sudden death after MI. The present work was designed to examine whether ABR deficiency affects angiogenesis in MI rats.
Baroreflex sensitivity (BRS) was determined in conscious rats at 1 month after occlusion of the left anterior descending coronary artery. The survival time was significantly shorter in Sprague-Dawley rats with BRS <0.60 ms/mmHg vs. those with BRS ≥0.60 ms/mmHg. Sinoaortic denervation destroyed ABR, and decreased capillary density, regional blood flow and vascular endothelial growth factor (VEGF) concentration after MI. Ketanserin (0.6 mg/kg/day) enhanced BRS, and increased capillary density, regional blood flow, and VEGF. Sinoaortic denervation also reduced the expression of vesicular acetylcholine (ACh) transporter and α7-nicotinic ACh receptor (α7-nAChR). Angiogenesis after MI was significantly attenuated in α7-nAChR knockout mice. In contrast, increase in endogenous ACh with cholinesterase inhibitor pyridostigmine (30 mg/kg/day) increased angiogenesis after MI. In cultured cardiac microvascular endothelial cells, ACh stimulated the expression of VEGF, phosphorylation of VEGF receptor 2, and tube formation in a manner dependent upon α7-nAChR.
Our results demonstrated that ABR deficiency could attenuate angiogenesis in ischaemic myocardium. These findings provide further mechanistic basis for enhancing baroreflex function in the treatment of MI.</abstract><cop>England</cop><pmid>21849351</pmid><doi>10.1093/eurheartj/ehr299</doi><tpages>9</tpages></addata></record> |
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| source | Oxford University Press Journals All Titles (1996-Current); MEDLINE; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | Acetylcholine - pharmacology Acetylcholine - physiology alpha7 Nicotinic Acetylcholine Receptor - metabolism alpha7 Nicotinic Acetylcholine Receptor - physiology Angiogenesis Inducing Agents - pharmacology Animals Baroreflex - physiology Blood Pressure - physiology Capillaries - physiology Cholinergic Agonists - pharmacology Cholinesterase Inhibitors - pharmacology Coronary Vessels - physiology Denervation - methods Ketanserin - pharmacology Mice Mice, Knockout Myocardial Infarction - physiopathology Neovascularization, Physiologic - physiology Pyridostigmine Bromide - pharmacology Rats Rats, Sprague-Dawley |
| title | Baroreflex deficiency hampers angiogenesis after myocardial infarction via acetylcholine-α7-nicotinic ACh receptor in rats |
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