Regulation of Endothelial Nitric Oxide Synthase by Tetrahydrobiopterin in Vascular Disease
ABSTRACT—Nitric oxide (NO), produced by endothelial nitric oxide synthase (eNOS), is a key signaling molecule in vascular homeostasis. Loss of NO bioavailability due to reduced synthesis and increased scavenging by reactive oxygen species is a cardinal feature of endothelial dysfunction in vascular...
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| Veröffentlicht in: | Arteriosclerosis, thrombosis, and vascular biology thrombosis, and vascular biology, 2004-03, Vol.24 (3), p.413-420 |
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| creator | Alp, Nicholas J Channon, Keith M |
| description | ABSTRACT—Nitric oxide (NO), produced by endothelial nitric oxide synthase (eNOS), is a key signaling molecule in vascular homeostasis. Loss of NO bioavailability due to reduced synthesis and increased scavenging by reactive oxygen species is a cardinal feature of endothelial dysfunction in vascular disease states. The pteridine cofactor tetrahydrobiopterin (BH4) has emerged as a critical determinant of eNOS activitywhen BH4 availability is limiting, eNOS no longer produces NO but instead generates superoxide. In vascular disease states, there is oxidative degradation of BH4 by reactive oxygen species. However, augmentation of BH4 concentrations in vascular disease by pharmacological supplementation, by enhancement of its rate of de novo biosynthesis or by measures to reduce its oxidation, has been shown in experimental studies to enhance NO bioavailability. Thus, BH4 represents a potential therapeutic target in the regulation of eNOS function in vascular disease. |
| doi_str_mv | 10.1161/01.ATV.0000110785.96039.f6 |
| format | Article |
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Loss of NO bioavailability due to reduced synthesis and increased scavenging by reactive oxygen species is a cardinal feature of endothelial dysfunction in vascular disease states. The pteridine cofactor tetrahydrobiopterin (BH4) has emerged as a critical determinant of eNOS activitywhen BH4 availability is limiting, eNOS no longer produces NO but instead generates superoxide. In vascular disease states, there is oxidative degradation of BH4 by reactive oxygen species. However, augmentation of BH4 concentrations in vascular disease by pharmacological supplementation, by enhancement of its rate of de novo biosynthesis or by measures to reduce its oxidation, has been shown in experimental studies to enhance NO bioavailability. Thus, BH4 represents a potential therapeutic target in the regulation of eNOS function in vascular disease.</description><identifier>ISSN: 1079-5642</identifier><identifier>EISSN: 1524-4636</identifier><identifier>DOI: 10.1161/01.ATV.0000110785.96039.f6</identifier><identifier>PMID: 14656731</identifier><identifier>CODEN: ATVBFA</identifier><language>eng</language><publisher>Philadelphia, PA: American Heart Association, Inc</publisher><subject>Animals ; Atherosclerosis (general aspects, experimental research) ; Biological and medical sciences ; Biological Availability ; Biopterins - analogs & derivatives ; Biopterins - physiology ; Biopterins - therapeutic use ; Blood and lymphatic vessels ; Cardiology. Vascular system ; Coenzymes - physiology ; Diabetes Mellitus - enzymology ; Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous ; Enzyme Induction ; GTP Cyclohydrolase - physiology ; Humans ; Hypercholesterolemia - enzymology ; Hypertension - enzymology ; Medical sciences ; Mice ; Mice, Mutant Strains ; Models, Animal ; Nitric Oxide - biosynthesis ; Nitric Oxide Synthase - metabolism ; Nitric Oxide Synthase Type II ; Nitric Oxide Synthase Type III ; Oxidation-Reduction ; Oxidative Stress ; Pterins - therapeutic use ; Rabbits ; Rats ; Rats, Inbred Strains ; Superoxides - metabolism ; Vascular Diseases - metabolism</subject><ispartof>Arteriosclerosis, thrombosis, and vascular biology, 2004-03, Vol.24 (3), p.413-420</ispartof><rights>2004 American Heart Association, Inc.</rights><rights>2004 INIST-CNRS</rights><rights>Copyright American Heart Association, Inc. 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Loss of NO bioavailability due to reduced synthesis and increased scavenging by reactive oxygen species is a cardinal feature of endothelial dysfunction in vascular disease states. The pteridine cofactor tetrahydrobiopterin (BH4) has emerged as a critical determinant of eNOS activitywhen BH4 availability is limiting, eNOS no longer produces NO but instead generates superoxide. In vascular disease states, there is oxidative degradation of BH4 by reactive oxygen species. However, augmentation of BH4 concentrations in vascular disease by pharmacological supplementation, by enhancement of its rate of de novo biosynthesis or by measures to reduce its oxidation, has been shown in experimental studies to enhance NO bioavailability. Thus, BH4 represents a potential therapeutic target in the regulation of eNOS function in vascular disease.</description><subject>Animals</subject><subject>Atherosclerosis (general aspects, experimental research)</subject><subject>Biological and medical sciences</subject><subject>Biological Availability</subject><subject>Biopterins - analogs & derivatives</subject><subject>Biopterins - physiology</subject><subject>Biopterins - therapeutic use</subject><subject>Blood and lymphatic vessels</subject><subject>Cardiology. Vascular system</subject><subject>Coenzymes - physiology</subject><subject>Diabetes Mellitus - enzymology</subject><subject>Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous</subject><subject>Enzyme Induction</subject><subject>GTP Cyclohydrolase - physiology</subject><subject>Humans</subject><subject>Hypercholesterolemia - enzymology</subject><subject>Hypertension - enzymology</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Mutant Strains</subject><subject>Models, Animal</subject><subject>Nitric Oxide - biosynthesis</subject><subject>Nitric Oxide Synthase - metabolism</subject><subject>Nitric Oxide Synthase Type II</subject><subject>Nitric Oxide Synthase Type III</subject><subject>Oxidation-Reduction</subject><subject>Oxidative Stress</subject><subject>Pterins - therapeutic use</subject><subject>Rabbits</subject><subject>Rats</subject><subject>Rats, Inbred Strains</subject><subject>Superoxides - metabolism</subject><subject>Vascular Diseases - metabolism</subject><issn>1079-5642</issn><issn>1524-4636</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkFtrFDEUgINY7EX_goSCjzPmnhnfSq1WKC20ax98CZlJ4qROJ9tkhrr_3rPuwoZATuA7tw-hc0pqShX9TGh9sXqsCRxKiW5k3SrC2zqoN-iESiYqobh6CzHRbSWVYMfotJQn4AVj5B06pkJJpTk9Qb_u_e9ltHNME04BX00uzYMfox3xbZxz7PHd3-g8fthM82CLx90Gr_yc7bBxOXUxrWef44ThPtrSQ6mMv8biAX2PjoIdi_-wf8_Qz29Xq8vr6ubu-4_Li5uql6rRFXcd8a1yQjjJqBS64512OnQNZzxoZhtFWKOcldS1VvaWEyFaWLDhIrSE8zN0vqu7zull8WU2T2nJE7Q0DBZulNQCoC87qM-plOyDWef4bPPGUGK2Vg2hBqyag1Xz36oJCpI_7jss3bN3h9S9RgA-7QFwYMeQ7dTHcuCkbEkjt6OKHfeaRvBW_ozLq89m8Hach21rwRWRFYOAcPhW22k0_weRjY9X</recordid><startdate>200403</startdate><enddate>200403</enddate><creator>Alp, Nicholas J</creator><creator>Channon, Keith M</creator><general>American Heart Association, Inc</general><general>Lippincott</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>K9.</scope></search><sort><creationdate>200403</creationdate><title>Regulation of Endothelial Nitric Oxide Synthase by Tetrahydrobiopterin in Vascular Disease</title><author>Alp, Nicholas J ; Channon, Keith M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5687-3db0e96d44d521547b3b7d7fb8323f72a860286da51d9a5ca30449636834f9033</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Animals</topic><topic>Atherosclerosis (general aspects, experimental research)</topic><topic>Biological and medical sciences</topic><topic>Biological Availability</topic><topic>Biopterins - analogs & derivatives</topic><topic>Biopterins - physiology</topic><topic>Biopterins - therapeutic use</topic><topic>Blood and lymphatic vessels</topic><topic>Cardiology. Vascular system</topic><topic>Coenzymes - physiology</topic><topic>Diabetes Mellitus - enzymology</topic><topic>Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous</topic><topic>Enzyme Induction</topic><topic>GTP Cyclohydrolase - physiology</topic><topic>Humans</topic><topic>Hypercholesterolemia - enzymology</topic><topic>Hypertension - enzymology</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Mutant Strains</topic><topic>Models, Animal</topic><topic>Nitric Oxide - biosynthesis</topic><topic>Nitric Oxide Synthase - metabolism</topic><topic>Nitric Oxide Synthase Type II</topic><topic>Nitric Oxide Synthase Type III</topic><topic>Oxidation-Reduction</topic><topic>Oxidative Stress</topic><topic>Pterins - therapeutic use</topic><topic>Rabbits</topic><topic>Rats</topic><topic>Rats, Inbred Strains</topic><topic>Superoxides - metabolism</topic><topic>Vascular Diseases - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Alp, Nicholas J</creatorcontrib><creatorcontrib>Channon, Keith M</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>ProQuest Health & Medical Complete (Alumni)</collection><jtitle>Arteriosclerosis, thrombosis, and vascular biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Alp, Nicholas J</au><au>Channon, Keith M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Regulation of Endothelial Nitric Oxide Synthase by Tetrahydrobiopterin in Vascular Disease</atitle><jtitle>Arteriosclerosis, thrombosis, and vascular biology</jtitle><addtitle>Arterioscler Thromb Vasc Biol</addtitle><date>2004-03</date><risdate>2004</risdate><volume>24</volume><issue>3</issue><spage>413</spage><epage>420</epage><pages>413-420</pages><issn>1079-5642</issn><eissn>1524-4636</eissn><coden>ATVBFA</coden><abstract>ABSTRACT—Nitric oxide (NO), produced by endothelial nitric oxide synthase (eNOS), is a key signaling molecule in vascular homeostasis. Loss of NO bioavailability due to reduced synthesis and increased scavenging by reactive oxygen species is a cardinal feature of endothelial dysfunction in vascular disease states. The pteridine cofactor tetrahydrobiopterin (BH4) has emerged as a critical determinant of eNOS activitywhen BH4 availability is limiting, eNOS no longer produces NO but instead generates superoxide. In vascular disease states, there is oxidative degradation of BH4 by reactive oxygen species. However, augmentation of BH4 concentrations in vascular disease by pharmacological supplementation, by enhancement of its rate of de novo biosynthesis or by measures to reduce its oxidation, has been shown in experimental studies to enhance NO bioavailability. Thus, BH4 represents a potential therapeutic target in the regulation of eNOS function in vascular disease.</abstract><cop>Philadelphia, PA</cop><cop>Hagerstown, MD</cop><pub>American Heart Association, Inc</pub><pmid>14656731</pmid><doi>10.1161/01.ATV.0000110785.96039.f6</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Atherosclerosis (general aspects, experimental research) Biological and medical sciences Biological Availability Biopterins - analogs & derivatives Biopterins - physiology Biopterins - therapeutic use Blood and lymphatic vessels Cardiology. Vascular system Coenzymes - physiology Diabetes Mellitus - enzymology Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous Enzyme Induction GTP Cyclohydrolase - physiology Humans Hypercholesterolemia - enzymology Hypertension - enzymology Medical sciences Mice Mice, Mutant Strains Models, Animal Nitric Oxide - biosynthesis Nitric Oxide Synthase - metabolism Nitric Oxide Synthase Type II Nitric Oxide Synthase Type III Oxidation-Reduction Oxidative Stress Pterins - therapeutic use Rabbits Rats Rats, Inbred Strains Superoxides - metabolism Vascular Diseases - metabolism |
| title | Regulation of Endothelial Nitric Oxide Synthase by Tetrahydrobiopterin in Vascular Disease |
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