Is smooth muscle growth in primate arteries regulated by endothelial nitric oxide synthase?
Purpose: We investigated whether control of constitutive endothelial cell nitric oxide synthase (cNOS) and nitric oxide (NO) by changes in shear stress might be important for the regulation of smooth muscle cell (SMC) growth and vascular diameter. Methods: Bilateral femoral arteriovenous fistulas we...
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| Veröffentlicht in: | Journal of vascular surgery 1998-09, Vol.28 (3), p.514-521 |
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| creator | Mattsson, Erney J.R. Geary, Randolph L. Kraiss, Larry W. Vergel, Selina Liao, James K. Corson, Marshall A. Au, Y.P.Tina Hanson, Stephen R. Clowes, Alexander W. |
| description | Purpose: We investigated whether control of constitutive endothelial cell nitric oxide synthase (cNOS) and nitric oxide (NO) by changes in shear stress might be important for the regulation of smooth muscle cell (SMC) growth and vascular diameter.
Methods: Bilateral femoral arteriovenous fistulas were placed in baboons to increase the blood flow in the external iliac arteries. At 2 months, the fistula was ligated on one side to restore normal flow (flow switch).
Results: In response to flow switch and a decrease in shear stress, iliac artery lumenal area decreased and SMC proliferation was induced. A decline in NO production, cNOS messenger RNA (mRNA), and protein were associated with these biological effects. In a subset of animals with iliac arteries under high flow, infusion of Nω-nitro-
l-arginine, an inhibitor of cNOS, did not induce proliferation.
Conclusion: Shear stress can regulate cNOS, vasoconstriction, and SMC proliferation. A decrease in nitric oxide may be necessary, but is not sufficient to induce SMC proliferation in response to a decrease in blood flow. (J Vasc Surg 1998:28:514-21.) |
| doi_str_mv | 10.1016/S0741-5214(98)70138-7 |
| format | Article |
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Methods: Bilateral femoral arteriovenous fistulas were placed in baboons to increase the blood flow in the external iliac arteries. At 2 months, the fistula was ligated on one side to restore normal flow (flow switch).
Results: In response to flow switch and a decrease in shear stress, iliac artery lumenal area decreased and SMC proliferation was induced. A decline in NO production, cNOS messenger RNA (mRNA), and protein were associated with these biological effects. In a subset of animals with iliac arteries under high flow, infusion of Nω-nitro-
l-arginine, an inhibitor of cNOS, did not induce proliferation.
Conclusion: Shear stress can regulate cNOS, vasoconstriction, and SMC proliferation. A decrease in nitric oxide may be necessary, but is not sufficient to induce SMC proliferation in response to a decrease in blood flow. (J Vasc Surg 1998:28:514-21.)</description><identifier>ISSN: 0741-5214</identifier><identifier>EISSN: 1097-6809</identifier><identifier>DOI: 10.1016/S0741-5214(98)70138-7</identifier><identifier>PMID: 9737462</identifier><identifier>CODEN: JVSUES</identifier><language>eng</language><publisher>New York, NY: Mosby, Inc</publisher><subject>Animals ; Biological and medical sciences ; Blood vessels and receptors ; Fundamental and applied biological sciences. Psychology ; Iliac Artery - cytology ; Male ; Muscle, Smooth, Vascular - cytology ; Muscle, Smooth, Vascular - physiology ; Nitric Oxide - physiology ; Nitric Oxide Synthase - genetics ; Nitric Oxide Synthase - physiology ; Nitric Oxide Synthase Type III ; Nitroarginine - pharmacology ; Papio ; RNA, Messenger - analysis ; Stress, Mechanical ; Vertebrates: cardiovascular system</subject><ispartof>Journal of vascular surgery, 1998-09, Vol.28 (3), p.514-521</ispartof><rights>1998 Society for Vascular Surgery and International Society for Cardiovascular Surgery, North American Chapter</rights><rights>1998 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c436t-f199852ecc783a128d96bb17678229b867c4318daa6d7d32cb7e30f35cf411183</citedby><cites>FETCH-LOGICAL-c436t-f199852ecc783a128d96bb17678229b867c4318daa6d7d32cb7e30f35cf411183</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/S0741-5214(98)70138-7$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>309,310,314,780,784,789,790,3550,23930,23931,25140,27924,27925,45995</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=2374400$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9737462$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Mattsson, Erney J.R.</creatorcontrib><creatorcontrib>Geary, Randolph L.</creatorcontrib><creatorcontrib>Kraiss, Larry W.</creatorcontrib><creatorcontrib>Vergel, Selina</creatorcontrib><creatorcontrib>Liao, James K.</creatorcontrib><creatorcontrib>Corson, Marshall A.</creatorcontrib><creatorcontrib>Au, Y.P.Tina</creatorcontrib><creatorcontrib>Hanson, Stephen R.</creatorcontrib><creatorcontrib>Clowes, Alexander W.</creatorcontrib><title>Is smooth muscle growth in primate arteries regulated by endothelial nitric oxide synthase?</title><title>Journal of vascular surgery</title><addtitle>J Vasc Surg</addtitle><description>Purpose: We investigated whether control of constitutive endothelial cell nitric oxide synthase (cNOS) and nitric oxide (NO) by changes in shear stress might be important for the regulation of smooth muscle cell (SMC) growth and vascular diameter.
Methods: Bilateral femoral arteriovenous fistulas were placed in baboons to increase the blood flow in the external iliac arteries. At 2 months, the fistula was ligated on one side to restore normal flow (flow switch).
Results: In response to flow switch and a decrease in shear stress, iliac artery lumenal area decreased and SMC proliferation was induced. A decline in NO production, cNOS messenger RNA (mRNA), and protein were associated with these biological effects. In a subset of animals with iliac arteries under high flow, infusion of Nω-nitro-
l-arginine, an inhibitor of cNOS, did not induce proliferation.
Conclusion: Shear stress can regulate cNOS, vasoconstriction, and SMC proliferation. A decrease in nitric oxide may be necessary, but is not sufficient to induce SMC proliferation in response to a decrease in blood flow. (J Vasc Surg 1998:28:514-21.)</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Blood vessels and receptors</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Iliac Artery - cytology</subject><subject>Male</subject><subject>Muscle, Smooth, Vascular - cytology</subject><subject>Muscle, Smooth, Vascular - physiology</subject><subject>Nitric Oxide - physiology</subject><subject>Nitric Oxide Synthase - genetics</subject><subject>Nitric Oxide Synthase - physiology</subject><subject>Nitric Oxide Synthase Type III</subject><subject>Nitroarginine - pharmacology</subject><subject>Papio</subject><subject>RNA, Messenger - analysis</subject><subject>Stress, Mechanical</subject><subject>Vertebrates: cardiovascular system</subject><issn>0741-5214</issn><issn>1097-6809</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1998</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkE1v1DAQhi0EarcLP6GSDxWih4AnTmL7VKGKfkiVOAAnDpZjT1pX-Wg9SWH_Pe7uaq-cLHue1zPzMHYK4jMIaL78EKqCoi6h-mT0uRIgdaHesBUIo4pGC_OWrQ7IMTshehQCoNbqiB0ZJVXVlCv2-5Y4DdM0P_BhId8jv0_Tn3yLI39KcXAzcpdmTBGJJ7xf-vwSeLvhOIacwj66no9xTtHz6W8MyGkzzg-O8OI9e9e5nvDD_lyzX1fffl7eFHffr28vv94VvpLNXHRgjK5L9F5p6aDUwTRtC6pRuixNqxuVOdDBuSaoIEvfKpSik7XvKgDQcs0-7v59StPzgjTbIZLHvncjTgtZJY2AKgtas3oH-jQRJezsdsW0sSDsq1S7lWpfjVmj7VZqjq_Z6b7B0g4YDqm9xVw_29cdedd3yY0-0gErM1UJkbGLHYZZxkvEZMlHHD2GmNDPNkzxP4P8A58Fk7s</recordid><startdate>19980901</startdate><enddate>19980901</enddate><creator>Mattsson, Erney J.R.</creator><creator>Geary, Randolph L.</creator><creator>Kraiss, Larry W.</creator><creator>Vergel, Selina</creator><creator>Liao, James K.</creator><creator>Corson, Marshall A.</creator><creator>Au, Y.P.Tina</creator><creator>Hanson, Stephen R.</creator><creator>Clowes, Alexander W.</creator><general>Mosby, Inc</general><general>Elsevier</general><scope>6I.</scope><scope>AAFTH</scope><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></search><sort><creationdate>19980901</creationdate><title>Is smooth muscle growth in primate arteries regulated by endothelial nitric oxide synthase?</title><author>Mattsson, Erney J.R. ; Geary, Randolph L. ; Kraiss, Larry W. ; Vergel, Selina ; Liao, James K. ; Corson, Marshall A. ; Au, Y.P.Tina ; Hanson, Stephen R. ; Clowes, Alexander W.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c436t-f199852ecc783a128d96bb17678229b867c4318daa6d7d32cb7e30f35cf411183</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1998</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Blood vessels and receptors</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Iliac Artery - cytology</topic><topic>Male</topic><topic>Muscle, Smooth, Vascular - cytology</topic><topic>Muscle, Smooth, Vascular - physiology</topic><topic>Nitric Oxide - physiology</topic><topic>Nitric Oxide Synthase - genetics</topic><topic>Nitric Oxide Synthase - physiology</topic><topic>Nitric Oxide Synthase Type III</topic><topic>Nitroarginine - pharmacology</topic><topic>Papio</topic><topic>RNA, Messenger - analysis</topic><topic>Stress, Mechanical</topic><topic>Vertebrates: cardiovascular system</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Mattsson, Erney J.R.</creatorcontrib><creatorcontrib>Geary, Randolph L.</creatorcontrib><creatorcontrib>Kraiss, Larry W.</creatorcontrib><creatorcontrib>Vergel, Selina</creatorcontrib><creatorcontrib>Liao, James K.</creatorcontrib><creatorcontrib>Corson, Marshall A.</creatorcontrib><creatorcontrib>Au, Y.P.Tina</creatorcontrib><creatorcontrib>Hanson, Stephen R.</creatorcontrib><creatorcontrib>Clowes, Alexander W.</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><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><jtitle>Journal of vascular surgery</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Mattsson, Erney J.R.</au><au>Geary, Randolph L.</au><au>Kraiss, Larry W.</au><au>Vergel, Selina</au><au>Liao, James K.</au><au>Corson, Marshall A.</au><au>Au, Y.P.Tina</au><au>Hanson, Stephen R.</au><au>Clowes, Alexander W.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Is smooth muscle growth in primate arteries regulated by endothelial nitric oxide synthase?</atitle><jtitle>Journal of vascular surgery</jtitle><addtitle>J Vasc Surg</addtitle><date>1998-09-01</date><risdate>1998</risdate><volume>28</volume><issue>3</issue><spage>514</spage><epage>521</epage><pages>514-521</pages><issn>0741-5214</issn><eissn>1097-6809</eissn><coden>JVSUES</coden><abstract>Purpose: We investigated whether control of constitutive endothelial cell nitric oxide synthase (cNOS) and nitric oxide (NO) by changes in shear stress might be important for the regulation of smooth muscle cell (SMC) growth and vascular diameter.
Methods: Bilateral femoral arteriovenous fistulas were placed in baboons to increase the blood flow in the external iliac arteries. At 2 months, the fistula was ligated on one side to restore normal flow (flow switch).
Results: In response to flow switch and a decrease in shear stress, iliac artery lumenal area decreased and SMC proliferation was induced. A decline in NO production, cNOS messenger RNA (mRNA), and protein were associated with these biological effects. In a subset of animals with iliac arteries under high flow, infusion of Nω-nitro-
l-arginine, an inhibitor of cNOS, did not induce proliferation.
Conclusion: Shear stress can regulate cNOS, vasoconstriction, and SMC proliferation. A decrease in nitric oxide may be necessary, but is not sufficient to induce SMC proliferation in response to a decrease in blood flow. (J Vasc Surg 1998:28:514-21.)</abstract><cop>New York, NY</cop><pub>Mosby, Inc</pub><pmid>9737462</pmid><doi>10.1016/S0741-5214(98)70138-7</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Access via ScienceDirect (Elsevier); EZB-FREE-00999 freely available EZB journals |
| subjects | Animals Biological and medical sciences Blood vessels and receptors Fundamental and applied biological sciences. Psychology Iliac Artery - cytology Male Muscle, Smooth, Vascular - cytology Muscle, Smooth, Vascular - physiology Nitric Oxide - physiology Nitric Oxide Synthase - genetics Nitric Oxide Synthase - physiology Nitric Oxide Synthase Type III Nitroarginine - pharmacology Papio RNA, Messenger - analysis Stress, Mechanical Vertebrates: cardiovascular system |
| title | Is smooth muscle growth in primate arteries regulated by endothelial nitric oxide synthase? |
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