Inhibition of Nitric Oxide Synthesis Potentiates Hypertension During Chronic Glucose Infusion in Rats
ABSTRACTEndothelial dysfunction has been proposed to contribute to impaired blood flow control or hypertension in many conditions characterized by hyperinsulinemia or hyperglycemia. However, most studies have focused on whether endothelial dysfunction is present in the established phases of these va...
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Veröffentlicht in: | Hypertension (Dallas, Tex. 1979) Tex. 1979), 2000-01, Vol.35 (1, Part 2 Suppl), p.451-451 |
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creator | Claxton, Christie R Brands, Michael W Fitzgerald, Sharyn M Cameron, Joseph A |
description | ABSTRACTEndothelial dysfunction has been proposed to contribute to impaired blood flow control or hypertension in many conditions characterized by hyperinsulinemia or hyperglycemia. However, most studies have focused on whether endothelial dysfunction is present in the established phases of these various hypertensive states, and there is little known concerning the role of the endothelium in the initial stages. This study tested whether nitric oxide production, before endothelial dysfunction develops, plays an important role in counteracting the hypertensive response to chronic glucose infusion. Glucose was infused (18.6 mg/kg per minute IV) for 7 days in 8 normal rats (G) and in 9 rats with a long-term background intravenous infusion of N-nitro-L-arginine methyl ester (L-NAME) at 10 μg/kg per minute (G+L). Mean arterial pressure (MAP), measured 24 hours per day, increased an average of ≈11 mm Hg in the G rats. L-NAME treatment increased MAP an average of 28±2 mm Hg in the G+L rats, and glucose infusion raised MAP >30 mm Hg above that, averaging 155±8 mm Hg by day 6. In addition, heart rate increased from an average of 389±8 bpm to 441±16 bpm by day 6, whereas there was no significant change in the G rats. Glomerular filtration rate decreased significantly with L-NAME treatment and decreased in both groups by day 3 of glucose infusion, reaching lower levels in the G+L rats. These results show that NO is required to minimize the increase in MAP during glucose infusion and suggest that renal and neural mechanisms may be important in mediating that effect. |
doi_str_mv | 10.1161/01.hyp.35.1.451 |
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However, most studies have focused on whether endothelial dysfunction is present in the established phases of these various hypertensive states, and there is little known concerning the role of the endothelium in the initial stages. This study tested whether nitric oxide production, before endothelial dysfunction develops, plays an important role in counteracting the hypertensive response to chronic glucose infusion. Glucose was infused (18.6 mg/kg per minute IV) for 7 days in 8 normal rats (G) and in 9 rats with a long-term background intravenous infusion of N-nitro-L-arginine methyl ester (L-NAME) at 10 μg/kg per minute (G+L). Mean arterial pressure (MAP), measured 24 hours per day, increased an average of ≈11 mm Hg in the G rats. L-NAME treatment increased MAP an average of 28±2 mm Hg in the G+L rats, and glucose infusion raised MAP >30 mm Hg above that, averaging 155±8 mm Hg by day 6. In addition, heart rate increased from an average of 389±8 bpm to 441±16 bpm by day 6, whereas there was no significant change in the G rats. Glomerular filtration rate decreased significantly with L-NAME treatment and decreased in both groups by day 3 of glucose infusion, reaching lower levels in the G+L rats. These results show that NO is required to minimize the increase in MAP during glucose infusion and suggest that renal and neural mechanisms may be important in mediating that effect.</description><identifier>ISSN: 0194-911X</identifier><identifier>EISSN: 1524-4563</identifier><identifier>DOI: 10.1161/01.hyp.35.1.451</identifier><identifier>PMID: 10642340</identifier><identifier>CODEN: HPRTDN</identifier><language>eng</language><publisher>United States: American Heart Association, Inc</publisher><subject>Animals ; Blood Glucose ; Blood Pressure - drug effects ; Endothelium, Vascular - enzymology ; Enzyme Inhibitors - pharmacology ; Glomerular Filtration Rate - drug effects ; Glucose - pharmacology ; Heart Rate - drug effects ; Hypertension - enzymology ; Infusions, Intravenous ; Insulin - blood ; Male ; NG-Nitroarginine Methyl Ester - pharmacology ; Nitric Oxide Synthase - antagonists & inhibitors ; Rats ; Rats, Sprague-Dawley ; Renin - blood</subject><ispartof>Hypertension (Dallas, Tex. 1979), 2000-01, Vol.35 (1, Part 2 Suppl), p.451-451</ispartof><rights>2000 American Heart Association, Inc.</rights><rights>Copyright American Heart Association, Inc. 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However, most studies have focused on whether endothelial dysfunction is present in the established phases of these various hypertensive states, and there is little known concerning the role of the endothelium in the initial stages. This study tested whether nitric oxide production, before endothelial dysfunction develops, plays an important role in counteracting the hypertensive response to chronic glucose infusion. Glucose was infused (18.6 mg/kg per minute IV) for 7 days in 8 normal rats (G) and in 9 rats with a long-term background intravenous infusion of N-nitro-L-arginine methyl ester (L-NAME) at 10 μg/kg per minute (G+L). Mean arterial pressure (MAP), measured 24 hours per day, increased an average of ≈11 mm Hg in the G rats. L-NAME treatment increased MAP an average of 28±2 mm Hg in the G+L rats, and glucose infusion raised MAP >30 mm Hg above that, averaging 155±8 mm Hg by day 6. In addition, heart rate increased from an average of 389±8 bpm to 441±16 bpm by day 6, whereas there was no significant change in the G rats. Glomerular filtration rate decreased significantly with L-NAME treatment and decreased in both groups by day 3 of glucose infusion, reaching lower levels in the G+L rats. These results show that NO is required to minimize the increase in MAP during glucose infusion and suggest that renal and neural mechanisms may be important in mediating that effect.</description><subject>Animals</subject><subject>Blood Glucose</subject><subject>Blood Pressure - drug effects</subject><subject>Endothelium, Vascular - enzymology</subject><subject>Enzyme Inhibitors - pharmacology</subject><subject>Glomerular Filtration Rate - drug effects</subject><subject>Glucose - pharmacology</subject><subject>Heart Rate - drug effects</subject><subject>Hypertension - enzymology</subject><subject>Infusions, Intravenous</subject><subject>Insulin - blood</subject><subject>Male</subject><subject>NG-Nitroarginine Methyl Ester - pharmacology</subject><subject>Nitric Oxide Synthase - antagonists & inhibitors</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Renin - blood</subject><issn>0194-911X</issn><issn>1524-4563</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2000</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkMtv1DAQxi0EotvCmRuyOHBL6okfiY9oge5KFa14SHCy8pgQl6y92I7K_vf1sj0gLMvj0fy-T6OPkFfASgAFlwzK6bAvuSyhFBKekBXIShRCKv6UrBhoUWiA72fkPMY7xkAIUT8nZ8CUqLhgK4JbN9nOJusd9SP9ZFOwPb35YwekXw4uTRhtpLc-oUu2TRjp5rDHkNt4lLxfgnU_6XoK3mXd1bz0PiLdunH5O7eOfm5TfEGeje0c8eVjvSDfPn74ut4U1zdX2_W766LnqoL8jqxpBoUg6141bc1qrYauGTWvpIK-aWXXcyEYAHZc5ylqrTtQ48jl0HX8grw9-e6D_71gTGZnY4_z3Dr0SzQ1a7RkQmbwzX_gnV-Cy7uZiknOBGdVhi5PUB98jAFHsw9214aDAWaO8RsGZvPj1nBpwOT4s-L1o-3S7XD4hz_lnQFxAu79nDDEX_Nyj8FM2M5pMiwfUammqI4_yLfINfs-AM9MkAg</recordid><startdate>200001</startdate><enddate>200001</enddate><creator>Claxton, Christie R</creator><creator>Brands, Michael W</creator><creator>Fitzgerald, Sharyn M</creator><creator>Cameron, Joseph A</creator><general>American Heart Association, Inc</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>K9.</scope><scope>7X8</scope></search><sort><creationdate>200001</creationdate><title>Inhibition of Nitric Oxide Synthesis Potentiates Hypertension During Chronic Glucose Infusion in Rats</title><author>Claxton, Christie R ; Brands, Michael W ; Fitzgerald, Sharyn M ; Cameron, Joseph A</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3621-c3f088d6e157c68a70796db8f932561c8a5bc344011eb39079e999b16ff35dbb3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2000</creationdate><topic>Animals</topic><topic>Blood Glucose</topic><topic>Blood Pressure - drug effects</topic><topic>Endothelium, Vascular - enzymology</topic><topic>Enzyme Inhibitors - pharmacology</topic><topic>Glomerular Filtration Rate - drug effects</topic><topic>Glucose - pharmacology</topic><topic>Heart Rate - drug effects</topic><topic>Hypertension - enzymology</topic><topic>Infusions, Intravenous</topic><topic>Insulin - blood</topic><topic>Male</topic><topic>NG-Nitroarginine Methyl Ester - pharmacology</topic><topic>Nitric Oxide Synthase - antagonists & inhibitors</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Renin - blood</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Claxton, Christie R</creatorcontrib><creatorcontrib>Brands, Michael W</creatorcontrib><creatorcontrib>Fitzgerald, Sharyn M</creatorcontrib><creatorcontrib>Cameron, Joseph 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>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><jtitle>Hypertension (Dallas, Tex. 1979)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Claxton, Christie R</au><au>Brands, Michael W</au><au>Fitzgerald, Sharyn M</au><au>Cameron, Joseph A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Inhibition of Nitric Oxide Synthesis Potentiates Hypertension During Chronic Glucose Infusion in Rats</atitle><jtitle>Hypertension (Dallas, Tex. 1979)</jtitle><addtitle>Hypertension</addtitle><date>2000-01</date><risdate>2000</risdate><volume>35</volume><issue>1, Part 2 Suppl</issue><spage>451</spage><epage>451</epage><pages>451-451</pages><issn>0194-911X</issn><eissn>1524-4563</eissn><coden>HPRTDN</coden><abstract>ABSTRACTEndothelial dysfunction has been proposed to contribute to impaired blood flow control or hypertension in many conditions characterized by hyperinsulinemia or hyperglycemia. 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subjects | Animals Blood Glucose Blood Pressure - drug effects Endothelium, Vascular - enzymology Enzyme Inhibitors - pharmacology Glomerular Filtration Rate - drug effects Glucose - pharmacology Heart Rate - drug effects Hypertension - enzymology Infusions, Intravenous Insulin - blood Male NG-Nitroarginine Methyl Ester - pharmacology Nitric Oxide Synthase - antagonists & inhibitors Rats Rats, Sprague-Dawley Renin - blood |
title | Inhibition of Nitric Oxide Synthesis Potentiates Hypertension During Chronic Glucose Infusion in Rats |
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