Progression of coronary and mesenteric vascular dysfunction in Zucker obese and Zucker diabetic fatty rats
Iowa Department of Veterans Affairs, Iowa City, Iowa; and Department of Internal Medicine, University of Iowa College of Medicine, Iowa City, Iowa Submitted 8 December 2005 ; accepted in final form 18 May 2006 We investigated the progression of vascular dysfunction associated with the metabolic synd...
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| Veröffentlicht in: | American journal of physiology. Heart and circulatory physiology 2006-10, Vol.291 (4), p.H1780-H1787 |
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| container_title | American journal of physiology. Heart and circulatory physiology |
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| creator | Oltman, Christine L Richou, Laura L Davidson, Eric P Coppey, Lawrence J Lund, Donald D Yorek, Mark A |
| description | Iowa Department of Veterans Affairs, Iowa City, Iowa; and Department of Internal Medicine, University of Iowa College of Medicine, Iowa City, Iowa
Submitted 8 December 2005
; accepted in final form 18 May 2006
We investigated the progression of vascular dysfunction associated with the metabolic syndrome with and without hyperglycemia in lean, Zucker obese, and Zucker diabetic fatty (ZDF) rats. Responses of aorta and small coronary and mesenteric arteries were measured to endothelium-dependent and -independent vasodilators. Indices of oxidative stress were increased in serum from ZDF rats throughout the study, whereas values were increased in Zucker obese rats later in the study [thiobarbituric acid reactive substances: 0.45 ± 0.02, 0.59 ± 0.03 ( P < 0.05), and 0.58 ± 0.03 ( P < 0.05) µg/ml in serum from 28- to 40-wk-old lean, Zucker obese, and ZDF rats, respectively]. Acetylcholine (ACh)-induced relaxation was not altered in vessels from lean animals from 840 wk. ACh-induced relaxation was nearly abolished in coronary arteries from 28- to 36-wk-old Zucker obese rats and by 1636 wk in ZDF rats and was attenuated in aorta and mesenteric vessels from ZDF rats [%relaxation to 10 µM ACh: 72.2 ± 7.1, 17.9 ± 5.9 ( P < 0.05), and 23.0 ± 4.5 ( P < 0.05) in coronary vessels; and 67.9 ± 9.2, 50.1 ± 5.5, and 42.3 ± 4.7 ( P < 0.05) in mesenteric vessels from 28- to 40-wk-old lean, Zucker obese, and ZDF rats, respectively]. The attenuated ACh-induced relaxation was improved when vessels were incubated with tiron, suggesting superoxide as a mechanism of endothelial dysfunction. Sodium nitroprusside-induced relaxation was not altered in aorta or coronary arteries and was potentiated in mesenteric arteries from Zucker obese rats. Our data suggest that diabetes enhances the progression of vascular dysfunction. Increases in indices of oxidative stress precede the development of dysfunction and may serve as a marker of endothelial damage.
metabolic syndrome; Type 2 diabetes; oxidative stress; acetylcholine
Address for reprint requests and other correspondence: C. L. Oltman, Cardiovascular Research, VA Medical Center, Rm. 204, Bld. 40, Highway 6 West, Iowa City, Iowa 52246 (e-mail: christine-oltman{at}uiowa.edu ) |
| doi_str_mv | 10.1152/ajpheart.01297.2005 |
| format | Article |
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Submitted 8 December 2005
; accepted in final form 18 May 2006
We investigated the progression of vascular dysfunction associated with the metabolic syndrome with and without hyperglycemia in lean, Zucker obese, and Zucker diabetic fatty (ZDF) rats. Responses of aorta and small coronary and mesenteric arteries were measured to endothelium-dependent and -independent vasodilators. Indices of oxidative stress were increased in serum from ZDF rats throughout the study, whereas values were increased in Zucker obese rats later in the study [thiobarbituric acid reactive substances: 0.45 ± 0.02, 0.59 ± 0.03 ( P < 0.05), and 0.58 ± 0.03 ( P < 0.05) µg/ml in serum from 28- to 40-wk-old lean, Zucker obese, and ZDF rats, respectively]. Acetylcholine (ACh)-induced relaxation was not altered in vessels from lean animals from 840 wk. ACh-induced relaxation was nearly abolished in coronary arteries from 28- to 36-wk-old Zucker obese rats and by 1636 wk in ZDF rats and was attenuated in aorta and mesenteric vessels from ZDF rats [%relaxation to 10 µM ACh: 72.2 ± 7.1, 17.9 ± 5.9 ( P < 0.05), and 23.0 ± 4.5 ( P < 0.05) in coronary vessels; and 67.9 ± 9.2, 50.1 ± 5.5, and 42.3 ± 4.7 ( P < 0.05) in mesenteric vessels from 28- to 40-wk-old lean, Zucker obese, and ZDF rats, respectively]. The attenuated ACh-induced relaxation was improved when vessels were incubated with tiron, suggesting superoxide as a mechanism of endothelial dysfunction. Sodium nitroprusside-induced relaxation was not altered in aorta or coronary arteries and was potentiated in mesenteric arteries from Zucker obese rats. Our data suggest that diabetes enhances the progression of vascular dysfunction. Increases in indices of oxidative stress precede the development of dysfunction and may serve as a marker of endothelial damage.
metabolic syndrome; Type 2 diabetes; oxidative stress; acetylcholine
Address for reprint requests and other correspondence: C. L. Oltman, Cardiovascular Research, VA Medical Center, Rm. 204, Bld. 40, Highway 6 West, Iowa City, Iowa 52246 (e-mail: christine-oltman{at}uiowa.edu )</description><identifier>ISSN: 0363-6135</identifier><identifier>EISSN: 1522-1539</identifier><identifier>DOI: 10.1152/ajpheart.01297.2005</identifier><identifier>PMID: 16714356</identifier><identifier>CODEN: AJPPDI</identifier><language>eng</language><publisher>United States: American Physiological Society</publisher><subject>Animals ; Cardiovascular Diseases - physiopathology ; Coronary vessels ; Coronary Vessels - drug effects ; Coronary Vessels - physiopathology ; Diabetes ; Diabetes Mellitus, Experimental - blood ; Diabetes Mellitus, Experimental - physiopathology ; Disease Progression ; Endothelium, Vascular - pathology ; Hyperglycemia - complications ; Insulin - blood ; Longitudinal Studies ; Mesenteric Arteries - drug effects ; Mesenteric Arteries - physiopathology ; Metabolic syndrome ; Metabolic Syndrome - blood ; Metabolic Syndrome - complications ; Metabolic Syndrome - physiopathology ; Neurotransmitters ; Nitroprusside - pharmacology ; Obesity - blood ; Obesity - physiopathology ; Oxidative Stress - physiology ; Rats ; Rats, Zucker ; Rodents ; Superoxides - metabolism ; Thiobarbituric Acid Reactive Substances - analysis ; Vasodilator Agents - pharmacology</subject><ispartof>American journal of physiology. Heart and circulatory physiology, 2006-10, Vol.291 (4), p.H1780-H1787</ispartof><rights>Copyright American Physiological Society Oct 2006</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c488t-117ee70771896ff774f5a85040e238a3e10c1177e6bb8e47fdbf4a58b018a8663</citedby><cites>FETCH-LOGICAL-c488t-117ee70771896ff774f5a85040e238a3e10c1177e6bb8e47fdbf4a58b018a8663</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,3039,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16714356$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Oltman, Christine L</creatorcontrib><creatorcontrib>Richou, Laura L</creatorcontrib><creatorcontrib>Davidson, Eric P</creatorcontrib><creatorcontrib>Coppey, Lawrence J</creatorcontrib><creatorcontrib>Lund, Donald D</creatorcontrib><creatorcontrib>Yorek, Mark A</creatorcontrib><title>Progression of coronary and mesenteric vascular dysfunction in Zucker obese and Zucker diabetic fatty rats</title><title>American journal of physiology. Heart and circulatory physiology</title><addtitle>Am J Physiol Heart Circ Physiol</addtitle><description>Iowa Department of Veterans Affairs, Iowa City, Iowa; and Department of Internal Medicine, University of Iowa College of Medicine, Iowa City, Iowa
Submitted 8 December 2005
; accepted in final form 18 May 2006
We investigated the progression of vascular dysfunction associated with the metabolic syndrome with and without hyperglycemia in lean, Zucker obese, and Zucker diabetic fatty (ZDF) rats. Responses of aorta and small coronary and mesenteric arteries were measured to endothelium-dependent and -independent vasodilators. Indices of oxidative stress were increased in serum from ZDF rats throughout the study, whereas values were increased in Zucker obese rats later in the study [thiobarbituric acid reactive substances: 0.45 ± 0.02, 0.59 ± 0.03 ( P < 0.05), and 0.58 ± 0.03 ( P < 0.05) µg/ml in serum from 28- to 40-wk-old lean, Zucker obese, and ZDF rats, respectively]. Acetylcholine (ACh)-induced relaxation was not altered in vessels from lean animals from 840 wk. ACh-induced relaxation was nearly abolished in coronary arteries from 28- to 36-wk-old Zucker obese rats and by 1636 wk in ZDF rats and was attenuated in aorta and mesenteric vessels from ZDF rats [%relaxation to 10 µM ACh: 72.2 ± 7.1, 17.9 ± 5.9 ( P < 0.05), and 23.0 ± 4.5 ( P < 0.05) in coronary vessels; and 67.9 ± 9.2, 50.1 ± 5.5, and 42.3 ± 4.7 ( P < 0.05) in mesenteric vessels from 28- to 40-wk-old lean, Zucker obese, and ZDF rats, respectively]. The attenuated ACh-induced relaxation was improved when vessels were incubated with tiron, suggesting superoxide as a mechanism of endothelial dysfunction. Sodium nitroprusside-induced relaxation was not altered in aorta or coronary arteries and was potentiated in mesenteric arteries from Zucker obese rats. Our data suggest that diabetes enhances the progression of vascular dysfunction. Increases in indices of oxidative stress precede the development of dysfunction and may serve as a marker of endothelial damage.
metabolic syndrome; Type 2 diabetes; oxidative stress; acetylcholine
Address for reprint requests and other correspondence: C. L. Oltman, Cardiovascular Research, VA Medical Center, Rm. 204, Bld. 40, Highway 6 West, Iowa City, Iowa 52246 (e-mail: christine-oltman{at}uiowa.edu )</description><subject>Animals</subject><subject>Cardiovascular Diseases - physiopathology</subject><subject>Coronary vessels</subject><subject>Coronary Vessels - drug effects</subject><subject>Coronary Vessels - physiopathology</subject><subject>Diabetes</subject><subject>Diabetes Mellitus, Experimental - blood</subject><subject>Diabetes Mellitus, Experimental - physiopathology</subject><subject>Disease Progression</subject><subject>Endothelium, Vascular - pathology</subject><subject>Hyperglycemia - complications</subject><subject>Insulin - blood</subject><subject>Longitudinal Studies</subject><subject>Mesenteric Arteries - drug effects</subject><subject>Mesenteric Arteries - physiopathology</subject><subject>Metabolic syndrome</subject><subject>Metabolic Syndrome - blood</subject><subject>Metabolic Syndrome - complications</subject><subject>Metabolic Syndrome - physiopathology</subject><subject>Neurotransmitters</subject><subject>Nitroprusside - pharmacology</subject><subject>Obesity - blood</subject><subject>Obesity - physiopathology</subject><subject>Oxidative Stress - physiology</subject><subject>Rats</subject><subject>Rats, Zucker</subject><subject>Rodents</subject><subject>Superoxides - metabolism</subject><subject>Thiobarbituric Acid Reactive Substances - analysis</subject><subject>Vasodilator Agents - pharmacology</subject><issn>0363-6135</issn><issn>1522-1539</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kU1v1DAQhi0EokvhFyAhiwO3bD1x_BFxQhWlSJXgUC5cLCcZ72bJxsF2Cvn3eLsLRUicLI2f59VoXkJeAlsDiPLC7qYt2pDWDMparUvGxCOyyj9lAYLXj8mKcckLCVyckWcx7lgmlORPyRlIBRUXckV2n4PfBIyx9yP1jrY--NGGhdqxo3uMOCYMfUvvbGznwQbaLdHNY5sOfD_Sr3P7DQP1TUbvndOg622DKYvOprTQYFN8Tp44O0R8cXrPyZer97eX18XNpw8fL9_dFG2ldSoAFKJiSoGupXNKVU5YLVjFsOTacgTWZkahbBqNlXJd4yordMNAWy0lPydvjrlT8N9njMns-9jiMNgR_RyN1FpwWesMvv4H3Pk5jHk3U5a1FAD8kMaPUBt8jAGdmUK_zxcywMyhB_O7B3Pfgzn0kK1Xp-i52WP34JwOn4GLI7DtN9sffUAzbZdcwuA3y0NiWYOpzDUozbLx9v_G1TwMt_gz_VH_Ms3UOf4LpjytFg</recordid><startdate>20061001</startdate><enddate>20061001</enddate><creator>Oltman, Christine L</creator><creator>Richou, Laura L</creator><creator>Davidson, Eric P</creator><creator>Coppey, Lawrence J</creator><creator>Lund, Donald D</creator><creator>Yorek, Mark A</creator><general>American Physiological Society</general><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>7QR</scope><scope>7TS</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>P64</scope><scope>7X8</scope></search><sort><creationdate>20061001</creationdate><title>Progression of coronary and mesenteric vascular dysfunction in Zucker obese and Zucker diabetic fatty rats</title><author>Oltman, Christine L ; Richou, Laura L ; Davidson, Eric P ; Coppey, Lawrence J ; Lund, Donald D ; Yorek, Mark A</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c488t-117ee70771896ff774f5a85040e238a3e10c1177e6bb8e47fdbf4a58b018a8663</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Animals</topic><topic>Cardiovascular Diseases - physiopathology</topic><topic>Coronary vessels</topic><topic>Coronary Vessels - drug effects</topic><topic>Coronary Vessels - physiopathology</topic><topic>Diabetes</topic><topic>Diabetes Mellitus, Experimental - blood</topic><topic>Diabetes Mellitus, Experimental - physiopathology</topic><topic>Disease Progression</topic><topic>Endothelium, Vascular - pathology</topic><topic>Hyperglycemia - complications</topic><topic>Insulin - blood</topic><topic>Longitudinal Studies</topic><topic>Mesenteric Arteries - drug effects</topic><topic>Mesenteric Arteries - physiopathology</topic><topic>Metabolic syndrome</topic><topic>Metabolic Syndrome - blood</topic><topic>Metabolic Syndrome - complications</topic><topic>Metabolic Syndrome - physiopathology</topic><topic>Neurotransmitters</topic><topic>Nitroprusside - pharmacology</topic><topic>Obesity - blood</topic><topic>Obesity - physiopathology</topic><topic>Oxidative Stress - physiology</topic><topic>Rats</topic><topic>Rats, Zucker</topic><topic>Rodents</topic><topic>Superoxides - metabolism</topic><topic>Thiobarbituric Acid Reactive Substances - analysis</topic><topic>Vasodilator Agents - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Oltman, Christine L</creatorcontrib><creatorcontrib>Richou, Laura L</creatorcontrib><creatorcontrib>Davidson, Eric P</creatorcontrib><creatorcontrib>Coppey, Lawrence J</creatorcontrib><creatorcontrib>Lund, Donald D</creatorcontrib><creatorcontrib>Yorek, Mark A</creatorcontrib><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>Chemoreception Abstracts</collection><collection>Physical Education Index</collection><collection>Toxicology Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>American journal of physiology. Heart and circulatory physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Oltman, Christine L</au><au>Richou, Laura L</au><au>Davidson, Eric P</au><au>Coppey, Lawrence J</au><au>Lund, Donald D</au><au>Yorek, Mark A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Progression of coronary and mesenteric vascular dysfunction in Zucker obese and Zucker diabetic fatty rats</atitle><jtitle>American journal of physiology. Heart and circulatory physiology</jtitle><addtitle>Am J Physiol Heart Circ Physiol</addtitle><date>2006-10-01</date><risdate>2006</risdate><volume>291</volume><issue>4</issue><spage>H1780</spage><epage>H1787</epage><pages>H1780-H1787</pages><issn>0363-6135</issn><eissn>1522-1539</eissn><coden>AJPPDI</coden><abstract>Iowa Department of Veterans Affairs, Iowa City, Iowa; and Department of Internal Medicine, University of Iowa College of Medicine, Iowa City, Iowa
Submitted 8 December 2005
; accepted in final form 18 May 2006
We investigated the progression of vascular dysfunction associated with the metabolic syndrome with and without hyperglycemia in lean, Zucker obese, and Zucker diabetic fatty (ZDF) rats. Responses of aorta and small coronary and mesenteric arteries were measured to endothelium-dependent and -independent vasodilators. Indices of oxidative stress were increased in serum from ZDF rats throughout the study, whereas values were increased in Zucker obese rats later in the study [thiobarbituric acid reactive substances: 0.45 ± 0.02, 0.59 ± 0.03 ( P < 0.05), and 0.58 ± 0.03 ( P < 0.05) µg/ml in serum from 28- to 40-wk-old lean, Zucker obese, and ZDF rats, respectively]. Acetylcholine (ACh)-induced relaxation was not altered in vessels from lean animals from 840 wk. ACh-induced relaxation was nearly abolished in coronary arteries from 28- to 36-wk-old Zucker obese rats and by 1636 wk in ZDF rats and was attenuated in aorta and mesenteric vessels from ZDF rats [%relaxation to 10 µM ACh: 72.2 ± 7.1, 17.9 ± 5.9 ( P < 0.05), and 23.0 ± 4.5 ( P < 0.05) in coronary vessels; and 67.9 ± 9.2, 50.1 ± 5.5, and 42.3 ± 4.7 ( P < 0.05) in mesenteric vessels from 28- to 40-wk-old lean, Zucker obese, and ZDF rats, respectively]. The attenuated ACh-induced relaxation was improved when vessels were incubated with tiron, suggesting superoxide as a mechanism of endothelial dysfunction. Sodium nitroprusside-induced relaxation was not altered in aorta or coronary arteries and was potentiated in mesenteric arteries from Zucker obese rats. Our data suggest that diabetes enhances the progression of vascular dysfunction. Increases in indices of oxidative stress precede the development of dysfunction and may serve as a marker of endothelial damage.
metabolic syndrome; Type 2 diabetes; oxidative stress; acetylcholine
Address for reprint requests and other correspondence: C. L. Oltman, Cardiovascular Research, VA Medical Center, Rm. 204, Bld. 40, Highway 6 West, Iowa City, Iowa 52246 (e-mail: christine-oltman{at}uiowa.edu )</abstract><cop>United States</cop><pub>American Physiological Society</pub><pmid>16714356</pmid><doi>10.1152/ajpheart.01297.2005</doi></addata></record> |
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| identifier | ISSN: 0363-6135 |
| ispartof | American journal of physiology. Heart and circulatory physiology, 2006-10, Vol.291 (4), p.H1780-H1787 |
| issn | 0363-6135 1522-1539 |
| language | eng |
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| source | MEDLINE; American Physiological Society Paid; EZB Electronic Journals Library |
| subjects | Animals Cardiovascular Diseases - physiopathology Coronary vessels Coronary Vessels - drug effects Coronary Vessels - physiopathology Diabetes Diabetes Mellitus, Experimental - blood Diabetes Mellitus, Experimental - physiopathology Disease Progression Endothelium, Vascular - pathology Hyperglycemia - complications Insulin - blood Longitudinal Studies Mesenteric Arteries - drug effects Mesenteric Arteries - physiopathology Metabolic syndrome Metabolic Syndrome - blood Metabolic Syndrome - complications Metabolic Syndrome - physiopathology Neurotransmitters Nitroprusside - pharmacology Obesity - blood Obesity - physiopathology Oxidative Stress - physiology Rats Rats, Zucker Rodents Superoxides - metabolism Thiobarbituric Acid Reactive Substances - analysis Vasodilator Agents - pharmacology |
| title | Progression of coronary and mesenteric vascular dysfunction in Zucker obese and Zucker diabetic fatty rats |
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