Effect of Epithelial Sodium Channel Blockade on the Myogenic Response of Rat Juxtamedullary Afferent Arterioles
The mechanotransduction mechanism underlying the myogenic response is poorly understood, but evidence implicates participation of epithelial sodium channel (ENaC)-like proteins. Therefore, the role of ENaC on the afferent arteriolar myogenic response was investigated in vitro using the blood-perfuse...
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| Veröffentlicht in: | Hypertension (Dallas, Tex. 1979) Tex. 1979), 2009-11, Vol.54 (5), p.1062-1069 |
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| creator | Guan, Zhengrong Pollock, Jennifer S Cook, Anthony K Hobbs, Janet L Inscho, Edward W |
| description | The mechanotransduction mechanism underlying the myogenic response is poorly understood, but evidence implicates participation of epithelial sodium channel (ENaC)-like proteins. Therefore, the role of ENaC on the afferent arteriolar myogenic response was investigated in vitro using the blood-perfused juxtamedullary nephron technique. Papillectomy was used to isolate myogenic influences by eliminating tubuloglomerular feedback signals. Autoregulatory responses were assessed by manipulating perfusion pressure in 30-mm Hg steps. Under control conditions, arteriolar diameter increased by 15% from 13.0±1.3 to 14.7±1.2 μm (P |
| doi_str_mv | 10.1161/HYPERTENSIONAHA.109.137992 |
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Therefore, the role of ENaC on the afferent arteriolar myogenic response was investigated in vitro using the blood-perfused juxtamedullary nephron technique. Papillectomy was used to isolate myogenic influences by eliminating tubuloglomerular feedback signals. Autoregulatory responses were assessed by manipulating perfusion pressure in 30-mm Hg steps. Under control conditions, arteriolar diameter increased by 15% from 13.0±1.3 to 14.7±1.2 μm (P<0.05) after reducing perfusion pressure from 100 to 70 mm Hg. Diameter decreased to 11.3±1.1 and 10.6±1.0 μm after increasing pressure to 130 and 160 mm Hg (88±1 and 81±2% of control diameter, P<0.05), respectively. Pressure-mediated autoregulatory responses were significantly inhibited by superfusion of 10 μmol/L amiloride (102±2, 97±4, and 94±3% of control diameter), or 10 μmol/L benzamil (106±5, 100±3, and 103±3% of control diameter), and when perfusing with blood containing 5 μmol/L amiloride (106±2, 97±4, and 97±4% of control diameter). Vasoconstrictor responses to 55 mmol/L KCl were preserved as diameters decreased by 67±4, 55±8, and 60±4% in afferent arterioles superfused with amiloride or benzamil, and perfused with amiloride, respectively. These responses were similar to responses obtained from control afferent arterioles (64±6%, P>0.05). Immunofluorescence revealed expression of the α, β, and γ subunits of ENaC in freshly isolated preglomerular microvascular smooth muscle cells. These results demonstrate that selective ENaC inhibitors attenuate afferent arteriolar myogenic responses and suggest that ENaC may function as mechanosensitive ion channels initiating pressure-dependent myogenic responses in rat juxtamedullary afferent arterioles.</description><identifier>ISSN: 0194-911X</identifier><identifier>EISSN: 1524-4563</identifier><identifier>DOI: 10.1161/HYPERTENSIONAHA.109.137992</identifier><identifier>PMID: 19720952</identifier><identifier>CODEN: HPRTDN</identifier><language>eng</language><publisher>Hagerstown, MD: American Heart Association, Inc</publisher><subject>Amiloride - analogs & derivatives ; Amiloride - pharmacology ; Analysis of Variance ; Animals ; Arterial hypertension. Arterial hypotension ; Arterioles - drug effects ; Arterioles - physiology ; Biological and medical sciences ; Blood and lymphatic vessels ; Cardiology. Vascular system ; Disease Models, Animal ; Experimental diseases ; Juxtaglomerular Apparatus - blood supply ; Juxtaglomerular Apparatus - drug effects ; Male ; Medical sciences ; Muscle, Smooth, Vascular - drug effects ; Muscle, Smooth, Vascular - physiology ; Probability ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Reference Values ; Sodium Channel Blockers - pharmacology ; Vasoconstriction - drug effects ; Vasodilation - drug effects</subject><ispartof>Hypertension (Dallas, Tex. 1979), 2009-11, Vol.54 (5), p.1062-1069</ispartof><rights>2009 American Heart Association, Inc.</rights><rights>2009 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5414-a2e88737dfb568c150797936bea2fa1f32c88e4ab0a91263abe93858e076bf383</citedby><cites>FETCH-LOGICAL-c5414-a2e88737dfb568c150797936bea2fa1f32c88e4ab0a91263abe93858e076bf383</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,315,781,785,886,3688,27926,27927</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=22058065$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19720952$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Guan, Zhengrong</creatorcontrib><creatorcontrib>Pollock, Jennifer S</creatorcontrib><creatorcontrib>Cook, Anthony K</creatorcontrib><creatorcontrib>Hobbs, Janet L</creatorcontrib><creatorcontrib>Inscho, Edward W</creatorcontrib><title>Effect of Epithelial Sodium Channel Blockade on the Myogenic Response of Rat Juxtamedullary Afferent Arterioles</title><title>Hypertension (Dallas, Tex. 1979)</title><addtitle>Hypertension</addtitle><description>The mechanotransduction mechanism underlying the myogenic response is poorly understood, but evidence implicates participation of epithelial sodium channel (ENaC)-like proteins. Therefore, the role of ENaC on the afferent arteriolar myogenic response was investigated in vitro using the blood-perfused juxtamedullary nephron technique. Papillectomy was used to isolate myogenic influences by eliminating tubuloglomerular feedback signals. Autoregulatory responses were assessed by manipulating perfusion pressure in 30-mm Hg steps. Under control conditions, arteriolar diameter increased by 15% from 13.0±1.3 to 14.7±1.2 μm (P<0.05) after reducing perfusion pressure from 100 to 70 mm Hg. Diameter decreased to 11.3±1.1 and 10.6±1.0 μm after increasing pressure to 130 and 160 mm Hg (88±1 and 81±2% of control diameter, P<0.05), respectively. Pressure-mediated autoregulatory responses were significantly inhibited by superfusion of 10 μmol/L amiloride (102±2, 97±4, and 94±3% of control diameter), or 10 μmol/L benzamil (106±5, 100±3, and 103±3% of control diameter), and when perfusing with blood containing 5 μmol/L amiloride (106±2, 97±4, and 97±4% of control diameter). Vasoconstrictor responses to 55 mmol/L KCl were preserved as diameters decreased by 67±4, 55±8, and 60±4% in afferent arterioles superfused with amiloride or benzamil, and perfused with amiloride, respectively. These responses were similar to responses obtained from control afferent arterioles (64±6%, P>0.05). Immunofluorescence revealed expression of the α, β, and γ subunits of ENaC in freshly isolated preglomerular microvascular smooth muscle cells. These results demonstrate that selective ENaC inhibitors attenuate afferent arteriolar myogenic responses and suggest that ENaC may function as mechanosensitive ion channels initiating pressure-dependent myogenic responses in rat juxtamedullary afferent arterioles.</description><subject>Amiloride - analogs & derivatives</subject><subject>Amiloride - pharmacology</subject><subject>Analysis of Variance</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>Cardiology. Vascular system</subject><subject>Disease Models, Animal</subject><subject>Experimental diseases</subject><subject>Juxtaglomerular Apparatus - blood supply</subject><subject>Juxtaglomerular Apparatus - drug effects</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Muscle, Smooth, Vascular - drug effects</subject><subject>Muscle, Smooth, Vascular - physiology</subject><subject>Probability</subject><subject>Random Allocation</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Reference Values</subject><subject>Sodium Channel Blockers - pharmacology</subject><subject>Vasoconstriction - drug effects</subject><subject>Vasodilation - drug effects</subject><issn>0194-911X</issn><issn>1524-4563</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkl1v0zAYhSMEYmXwF5CFBHcptuP4gwukUGV0aGyoGxJcWY77Zglz42InG_v3uGo1PixZlu3nPT72cZa9InhOCCdvl9-_1Kur-vzy9OK8WlZzgtWcFEIp-iibkZKynJW8eJzNMFEsV4R8O8qexfgDY8IYE0-zI6IExaqks8zXbQt2RL5F9bYfO3C9cejSr_tpgxadGQZw6IPz9sasAfkBJQR9vvfXMPQWrSBu_RBhV74yI_o0_RrNBtaTcybcoyppBxhGVIURQu8dxOfZk9a4CC8O43H29aS-Wizzs4uPp4vqLLclIyw3FKQUhVi3TcmlJSUWSqiCN2Boa0hbUCslMNNgowjlhWlAFbKUgAVv2kIWx9n7ve52apIhm1wE4_Q29JvkTHvT6393hr7T1_5WU8E5JjgJvDkIBP9zgjjqTR8tpIsN4KeoueCKSLED3-1BG3yMAdqHQwjWu7z0f3mldaX3eaXil3_b_FN6CCgBrw-Aida4NpjB9vGBoxSXEvMycWzP3XmX3jreuOkOgu7AuLHTODVGucwpxuk_pFmeOmXFb8YIsiY</recordid><startdate>200911</startdate><enddate>200911</enddate><creator>Guan, Zhengrong</creator><creator>Pollock, Jennifer S</creator><creator>Cook, Anthony K</creator><creator>Hobbs, Janet L</creator><creator>Inscho, Edward W</creator><general>American Heart Association, Inc</general><general>Lippincott Williams & Wilkins</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>7X8</scope><scope>5PM</scope></search><sort><creationdate>200911</creationdate><title>Effect of Epithelial Sodium Channel Blockade on the Myogenic Response of Rat Juxtamedullary Afferent Arterioles</title><author>Guan, Zhengrong ; Pollock, Jennifer S ; Cook, Anthony K ; Hobbs, Janet L ; Inscho, Edward W</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5414-a2e88737dfb568c150797936bea2fa1f32c88e4ab0a91263abe93858e076bf383</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Amiloride - analogs & derivatives</topic><topic>Amiloride - pharmacology</topic><topic>Analysis of Variance</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>Cardiology. Vascular system</topic><topic>Disease Models, Animal</topic><topic>Experimental diseases</topic><topic>Juxtaglomerular Apparatus - blood supply</topic><topic>Juxtaglomerular Apparatus - drug effects</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Muscle, Smooth, Vascular - drug effects</topic><topic>Muscle, Smooth, Vascular - physiology</topic><topic>Probability</topic><topic>Random Allocation</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Reference Values</topic><topic>Sodium Channel Blockers - pharmacology</topic><topic>Vasoconstriction - drug effects</topic><topic>Vasodilation - drug effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Guan, Zhengrong</creatorcontrib><creatorcontrib>Pollock, Jennifer S</creatorcontrib><creatorcontrib>Cook, Anthony K</creatorcontrib><creatorcontrib>Hobbs, Janet L</creatorcontrib><creatorcontrib>Inscho, Edward W</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>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Hypertension (Dallas, Tex. 1979)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Guan, Zhengrong</au><au>Pollock, Jennifer S</au><au>Cook, Anthony K</au><au>Hobbs, Janet L</au><au>Inscho, Edward W</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effect of Epithelial Sodium Channel Blockade on the Myogenic Response of Rat Juxtamedullary Afferent Arterioles</atitle><jtitle>Hypertension (Dallas, Tex. 1979)</jtitle><addtitle>Hypertension</addtitle><date>2009-11</date><risdate>2009</risdate><volume>54</volume><issue>5</issue><spage>1062</spage><epage>1069</epage><pages>1062-1069</pages><issn>0194-911X</issn><eissn>1524-4563</eissn><coden>HPRTDN</coden><abstract>The mechanotransduction mechanism underlying the myogenic response is poorly understood, but evidence implicates participation of epithelial sodium channel (ENaC)-like proteins. Therefore, the role of ENaC on the afferent arteriolar myogenic response was investigated in vitro using the blood-perfused juxtamedullary nephron technique. Papillectomy was used to isolate myogenic influences by eliminating tubuloglomerular feedback signals. Autoregulatory responses were assessed by manipulating perfusion pressure in 30-mm Hg steps. Under control conditions, arteriolar diameter increased by 15% from 13.0±1.3 to 14.7±1.2 μm (P<0.05) after reducing perfusion pressure from 100 to 70 mm Hg. Diameter decreased to 11.3±1.1 and 10.6±1.0 μm after increasing pressure to 130 and 160 mm Hg (88±1 and 81±2% of control diameter, P<0.05), respectively. Pressure-mediated autoregulatory responses were significantly inhibited by superfusion of 10 μmol/L amiloride (102±2, 97±4, and 94±3% of control diameter), or 10 μmol/L benzamil (106±5, 100±3, and 103±3% of control diameter), and when perfusing with blood containing 5 μmol/L amiloride (106±2, 97±4, and 97±4% of control diameter). Vasoconstrictor responses to 55 mmol/L KCl were preserved as diameters decreased by 67±4, 55±8, and 60±4% in afferent arterioles superfused with amiloride or benzamil, and perfused with amiloride, respectively. These responses were similar to responses obtained from control afferent arterioles (64±6%, P>0.05). Immunofluorescence revealed expression of the α, β, and γ subunits of ENaC in freshly isolated preglomerular microvascular smooth muscle cells. These results demonstrate that selective ENaC inhibitors attenuate afferent arteriolar myogenic responses and suggest that ENaC may function as mechanosensitive ion channels initiating pressure-dependent myogenic responses in rat juxtamedullary afferent arterioles.</abstract><cop>Hagerstown, MD</cop><pub>American Heart Association, Inc</pub><pmid>19720952</pmid><doi>10.1161/HYPERTENSIONAHA.109.137992</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Hypertension (Dallas, Tex. 1979), 2009-11, Vol.54 (5), p.1062-1069 |
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| source | MEDLINE; American Heart Association Journals; Journals@Ovid Complete; EZB-FREE-00999 freely available EZB journals |
| subjects | Amiloride - analogs & derivatives Amiloride - pharmacology Analysis of Variance Animals Arterial hypertension. Arterial hypotension Arterioles - drug effects Arterioles - physiology Biological and medical sciences Blood and lymphatic vessels Cardiology. Vascular system Disease Models, Animal Experimental diseases Juxtaglomerular Apparatus - blood supply Juxtaglomerular Apparatus - drug effects Male Medical sciences Muscle, Smooth, Vascular - drug effects Muscle, Smooth, Vascular - physiology Probability Random Allocation Rats Rats, Sprague-Dawley Reference Values Sodium Channel Blockers - pharmacology Vasoconstriction - drug effects Vasodilation - drug effects |
| title | Effect of Epithelial Sodium Channel Blockade on the Myogenic Response of Rat Juxtamedullary Afferent Arterioles |
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