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Impaired Conduction of Vasodilation Along Arterioles in Connexin40-Deficient Mice
ABSTRACTConnexins have been hypothesized to play an important role in intercellular communication within the vascular wall and may provide a mechanistic explanation for conduction of vasomotor responses. To test this hypothesis, we studied the transmission of vasomotor responses in the intact skelet...
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| Published in: | Circulation research 2000-03, Vol.86 (6), p.649-655 |
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| container_title | Circulation research |
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| creator | de Wit, Cor Roos, Frederik Bolz, Steffen-Sebastian Kirchhoff, Susanne Krüger, Olaf Willecke, Klaus Pohl, Ulrich |
| description | ABSTRACTConnexins have been hypothesized to play an important role in intercellular communication within the vascular wall and may provide a mechanistic explanation for conduction of vasomotor responses. To test this hypothesis, we studied the transmission of vasomotor responses in the intact skeletal muscle microcirculation of connexin40-deficient mice (Cx40). Arterioles were locally stimulated with hyperpolarizing dilators (acetylcholine [ACh] as well as bradykinin [Bk]) or depolarizing K solution, and the resulting changes in diameter were measured using a videomicroscopy technique at the site of application and up to 1.32 mm upstream. Arterial pressure was elevated 25% in Cx40 mice (94±5 versus 75±4 mm Hg). Vessels selected for study had equivalent basal diameter and vasomotor tone in both genotypes of mice. Vasomotion was present in small arterioles of both genotypes, but its intensity was exaggerated in Cx40 mice. ACh and Bk induced dilation (33% and 53%, respectively, of maximal response) at the site of application that was of similar magnitude in both genotypes. These dilations were observed to spread upstream within |
| doi_str_mv | 10.1161/01.res.86.6.649 |
| format | article |
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To test this hypothesis, we studied the transmission of vasomotor responses in the intact skeletal muscle microcirculation of connexin40-deficient mice (Cx40). Arterioles were locally stimulated with hyperpolarizing dilators (acetylcholine [ACh] as well as bradykinin [Bk]) or depolarizing K solution, and the resulting changes in diameter were measured using a videomicroscopy technique at the site of application and up to 1.32 mm upstream. Arterial pressure was elevated 25% in Cx40 mice (94±5 versus 75±4 mm Hg). Vessels selected for study had equivalent basal diameter and vasomotor tone in both genotypes of mice. Vasomotion was present in small arterioles of both genotypes, but its intensity was exaggerated in Cx40 mice. ACh and Bk induced dilation (33% and 53%, respectively, of maximal response) at the site of application that was of similar magnitude in both genotypes. These dilations were observed to spread upstream within <1 second without significant attenuation in Cx40 mice. However, spreading was severely attenuated in Cx40 animals (11±4% versus 35±7% with ACh and 38±5% versus 60±7% with Bk in Cx40 and Cx40, respectively;P <0.05). In contrast, conducted vasoconstrictions, induced by K solution decreased equally with distance in both genotypes. These results support a significant role for Cx40 in vascular intercellular communication. Our observations indicate that Cx40 is required for normal transmission of endothelium-dependent vasodilator responses and may underlie altered vasomotion patterns.</description><identifier>ISSN: 0009-7330</identifier><identifier>EISSN: 1524-4571</identifier><identifier>DOI: 10.1161/01.res.86.6.649</identifier><identifier>PMID: 10747000</identifier><identifier>CODEN: CIRUAL</identifier><language>eng</language><publisher>Hagerstown, MD: American Heart Association, Inc</publisher><subject>Acetylcholine - pharmacology ; Animals ; Arterial hypertension. Arterial hypotension ; Arterioles - drug effects ; Arterioles - physiology ; Biological and medical sciences ; Blood and lymphatic vessels ; Blood Pressure - physiology ; Bradykinin - pharmacology ; Cardiology. Vascular system ; Connexins - deficiency ; Connexins - physiology ; Experimental diseases ; Gap Junction alpha-5 Protein ; Medical sciences ; Mice ; Potassium - pharmacology ; Vasodilation - physiology ; Vasodilator Agents - pharmacology ; Vasomotor System - physiology</subject><ispartof>Circulation research, 2000-03, Vol.86 (6), p.649-655</ispartof><rights>2000 American Heart Association, Inc.</rights><rights>2000 INIST-CNRS</rights><rights>Copyright American Heart Association, Inc. Mar 31, 2000</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5839-9d1e32b09ae232e63867e44571d9689d1aaae28f38df6b2392297acdaf43a7d23</citedby><cites>FETCH-LOGICAL-c5839-9d1e32b09ae232e63867e44571d9689d1aaae28f38df6b2392297acdaf43a7d23</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1339703$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10747000$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>de Wit, Cor</creatorcontrib><creatorcontrib>Roos, Frederik</creatorcontrib><creatorcontrib>Bolz, Steffen-Sebastian</creatorcontrib><creatorcontrib>Kirchhoff, Susanne</creatorcontrib><creatorcontrib>Krüger, Olaf</creatorcontrib><creatorcontrib>Willecke, Klaus</creatorcontrib><creatorcontrib>Pohl, Ulrich</creatorcontrib><title>Impaired Conduction of Vasodilation Along Arterioles in Connexin40-Deficient Mice</title><title>Circulation research</title><addtitle>Circ Res</addtitle><description>ABSTRACTConnexins have been hypothesized to play an important role in intercellular communication within the vascular wall and may provide a mechanistic explanation for conduction of vasomotor responses. To test this hypothesis, we studied the transmission of vasomotor responses in the intact skeletal muscle microcirculation of connexin40-deficient mice (Cx40). Arterioles were locally stimulated with hyperpolarizing dilators (acetylcholine [ACh] as well as bradykinin [Bk]) or depolarizing K solution, and the resulting changes in diameter were measured using a videomicroscopy technique at the site of application and up to 1.32 mm upstream. Arterial pressure was elevated 25% in Cx40 mice (94±5 versus 75±4 mm Hg). Vessels selected for study had equivalent basal diameter and vasomotor tone in both genotypes of mice. Vasomotion was present in small arterioles of both genotypes, but its intensity was exaggerated in Cx40 mice. ACh and Bk induced dilation (33% and 53%, respectively, of maximal response) at the site of application that was of similar magnitude in both genotypes. These dilations were observed to spread upstream within <1 second without significant attenuation in Cx40 mice. However, spreading was severely attenuated in Cx40 animals (11±4% versus 35±7% with ACh and 38±5% versus 60±7% with Bk in Cx40 and Cx40, respectively;P <0.05). In contrast, conducted vasoconstrictions, induced by K solution decreased equally with distance in both genotypes. These results support a significant role for Cx40 in vascular intercellular communication. Our observations indicate that Cx40 is required for normal transmission of endothelium-dependent vasodilator responses and may underlie altered vasomotion patterns.</description><subject>Acetylcholine - pharmacology</subject><subject>Animals</subject><subject>Arterial hypertension. Arterial hypotension</subject><subject>Arterioles - drug effects</subject><subject>Arterioles - physiology</subject><subject>Biological and medical sciences</subject><subject>Blood and lymphatic vessels</subject><subject>Blood Pressure - physiology</subject><subject>Bradykinin - pharmacology</subject><subject>Cardiology. Vascular system</subject><subject>Connexins - deficiency</subject><subject>Connexins - physiology</subject><subject>Experimental diseases</subject><subject>Gap Junction alpha-5 Protein</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Potassium - pharmacology</subject><subject>Vasodilation - physiology</subject><subject>Vasodilator Agents - pharmacology</subject><subject>Vasomotor System - physiology</subject><issn>0009-7330</issn><issn>1524-4571</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2000</creationdate><recordtype>article</recordtype><recordid>eNpdkM1vEzEQxS0EomnhzA2tEOK26fgja_sYhVIqFSE-r5aznqUujp3auyr893ibSCA0hxnr_eZ59Ah5QWFJaUfPgS4zlqXqlrWEfkQWdMVEK1aSPiYLANCt5BxOyGkptwBUcKafkhMKUsiqLsinq93e-oyu2aTopn70KTZpaL7bkpwP9uG9Din-aNZ5xOxTwNL4OOMRf_kooH2Lg-89xrH54Ht8Rp4MNhR8fuxn5Nu7i6-b9-31x8urzfq67VeK61Y7ipxtQVtknGHHVSdRzIc73amqWlsVNXDlhm7LuGZMS9s7OwhupWP8jLw5-O5zupuwjGbnS48h2IhpKkZSoFIJXsFX_4G3acqx3mYYZYKupJqh8wPU51RKxsHss9_Z_NtQMHPUBqj5fPHFqM7UErpuvDzaTtsdun_4Q7YVeH0EbOltGLKNvS9_Oc61hPlnccDuU6gBl59husdsbtCG8cbA7ASUtexh4hTaedD8D96tlJs</recordid><startdate>20000331</startdate><enddate>20000331</enddate><creator>de Wit, Cor</creator><creator>Roos, Frederik</creator><creator>Bolz, Steffen-Sebastian</creator><creator>Kirchhoff, Susanne</creator><creator>Krüger, Olaf</creator><creator>Willecke, Klaus</creator><creator>Pohl, Ulrich</creator><general>American Heart Association, Inc</general><general>Lippincott</general><general>Lippincott Williams & Wilkins Ovid Technologies</general><scope>IQODW</scope><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>7QP</scope><scope>7T5</scope><scope>7TK</scope><scope>H94</scope><scope>K9.</scope><scope>7X8</scope></search><sort><creationdate>20000331</creationdate><title>Impaired Conduction of Vasodilation Along Arterioles in Connexin40-Deficient Mice</title><author>de Wit, Cor ; Roos, Frederik ; Bolz, Steffen-Sebastian ; Kirchhoff, Susanne ; Krüger, Olaf ; Willecke, Klaus ; Pohl, Ulrich</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5839-9d1e32b09ae232e63867e44571d9689d1aaae28f38df6b2392297acdaf43a7d23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2000</creationdate><topic>Acetylcholine - pharmacology</topic><topic>Animals</topic><topic>Arterial hypertension. Arterial hypotension</topic><topic>Arterioles - drug effects</topic><topic>Arterioles - physiology</topic><topic>Biological and medical sciences</topic><topic>Blood and lymphatic vessels</topic><topic>Blood Pressure - physiology</topic><topic>Bradykinin - pharmacology</topic><topic>Cardiology. Vascular system</topic><topic>Connexins - deficiency</topic><topic>Connexins - physiology</topic><topic>Experimental diseases</topic><topic>Gap Junction alpha-5 Protein</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Potassium - pharmacology</topic><topic>Vasodilation - physiology</topic><topic>Vasodilator Agents - pharmacology</topic><topic>Vasomotor System - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>de Wit, Cor</creatorcontrib><creatorcontrib>Roos, Frederik</creatorcontrib><creatorcontrib>Bolz, Steffen-Sebastian</creatorcontrib><creatorcontrib>Kirchhoff, Susanne</creatorcontrib><creatorcontrib>Krüger, Olaf</creatorcontrib><creatorcontrib>Willecke, Klaus</creatorcontrib><creatorcontrib>Pohl, Ulrich</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><jtitle>Circulation research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>de Wit, Cor</au><au>Roos, Frederik</au><au>Bolz, Steffen-Sebastian</au><au>Kirchhoff, Susanne</au><au>Krüger, Olaf</au><au>Willecke, Klaus</au><au>Pohl, Ulrich</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Impaired Conduction of Vasodilation Along Arterioles in Connexin40-Deficient Mice</atitle><jtitle>Circulation research</jtitle><addtitle>Circ Res</addtitle><date>2000-03-31</date><risdate>2000</risdate><volume>86</volume><issue>6</issue><spage>649</spage><epage>655</epage><pages>649-655</pages><issn>0009-7330</issn><eissn>1524-4571</eissn><coden>CIRUAL</coden><abstract>ABSTRACTConnexins have been hypothesized to play an important role in intercellular communication within the vascular wall and may provide a mechanistic explanation for conduction of vasomotor responses. To test this hypothesis, we studied the transmission of vasomotor responses in the intact skeletal muscle microcirculation of connexin40-deficient mice (Cx40). Arterioles were locally stimulated with hyperpolarizing dilators (acetylcholine [ACh] as well as bradykinin [Bk]) or depolarizing K solution, and the resulting changes in diameter were measured using a videomicroscopy technique at the site of application and up to 1.32 mm upstream. Arterial pressure was elevated 25% in Cx40 mice (94±5 versus 75±4 mm Hg). Vessels selected for study had equivalent basal diameter and vasomotor tone in both genotypes of mice. Vasomotion was present in small arterioles of both genotypes, but its intensity was exaggerated in Cx40 mice. ACh and Bk induced dilation (33% and 53%, respectively, of maximal response) at the site of application that was of similar magnitude in both genotypes. These dilations were observed to spread upstream within <1 second without significant attenuation in Cx40 mice. However, spreading was severely attenuated in Cx40 animals (11±4% versus 35±7% with ACh and 38±5% versus 60±7% with Bk in Cx40 and Cx40, respectively;P <0.05). In contrast, conducted vasoconstrictions, induced by K solution decreased equally with distance in both genotypes. These results support a significant role for Cx40 in vascular intercellular communication. Our observations indicate that Cx40 is required for normal transmission of endothelium-dependent vasodilator responses and may underlie altered vasomotion patterns.</abstract><cop>Hagerstown, MD</cop><pub>American Heart Association, Inc</pub><pmid>10747000</pmid><doi>10.1161/01.res.86.6.649</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Circulation research, 2000-03, Vol.86 (6), p.649-655 |
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| language | eng |
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| source | Freely Accessible Science Journals - check A-Z of ejournals |
| subjects | Acetylcholine - pharmacology Animals Arterial hypertension. Arterial hypotension Arterioles - drug effects Arterioles - physiology Biological and medical sciences Blood and lymphatic vessels Blood Pressure - physiology Bradykinin - pharmacology Cardiology. Vascular system Connexins - deficiency Connexins - physiology Experimental diseases Gap Junction alpha-5 Protein Medical sciences Mice Potassium - pharmacology Vasodilation - physiology Vasodilator Agents - pharmacology Vasomotor System - physiology |
| title | Impaired Conduction of Vasodilation Along Arterioles in Connexin40-Deficient Mice |
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