Sodium molybdate prevents hypertension and vascular prostanoid imbalance in fructose-overloaded rats
Summary Fructose (F) overload produces elevated blood pressure (BP), hyperglycaemia, hypertriglyceridemia and insulin resistance, resembling human metabolic syndrome. Previously, we found altered vascular prostanoid (PR) production in this model. Sodium molybdate (Mo), as well as sodium tungstate, c...
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| Veröffentlicht in: | Autonomic & autacoid pharmacology 2013-10, Vol.33 (3-4), p.43-48 |
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| container_title | Autonomic & autacoid pharmacology |
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| creator | Peredo, H. A. Andrade, V. Donoso, A. S. Lee, H. J. Puyó, A. M. |
| description | Summary
Fructose (F) overload produces elevated blood pressure (BP), hyperglycaemia, hypertriglyceridemia and insulin resistance, resembling human metabolic syndrome. Previously, we found altered vascular prostanoid (PR) production in this model.
Sodium molybdate (Mo), as well as sodium tungstate, causes insulin‐like effects and normalizes plasma glucose levels in streptozotocin‐treated diabetic rats. We studied the effects of Mo on BP, metabolic parameters and release of PR from the mesenteric vascular bed (MVB) in F‐overloaded rats.
Four groups of male Sprague‐Dawley rats were analysed: Control, tap water to drink; F, F solution 10% W/V to drink; CMo, Mo 100 mg kg day−1 and FMo, both treatments. After 9 weeks, the animals were killed and MVBs removed and the released PRs measured.
F increased BP, glycemia, triglyceridemia and insulinemia. Mo treatment prevented the increases in BP and glycemia, but did not modify triglyceridemia or insulinemia. In addition, Mo decreased BP in controls.
Prostaglandins (PG) F2alpha and E2, PG 6‐ketoF1alpha and thromboxane (TX) B2, as well as inactive metabolites of prostacyclin (PGI2) and TXA2 were detected. F decreased the production of vasodilator PRs PGI2 and PGE2 in MVB. Mo prevented these alterations and increased PGE2 in controls. Vasoconstrict or PRs PGF2alpha and TXA2 release was not modified.
Mo treatment, beyond its known lowering effect on glycemia, prevents the reduction in the vascular release of vasodilator PR observed in this model. This could be one of the mechanisms by which Mo avoids the increase in BP caused by F overload in the rat. |
| doi_str_mv | 10.1111/aap.12010 |
| format | Article |
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Fructose (F) overload produces elevated blood pressure (BP), hyperglycaemia, hypertriglyceridemia and insulin resistance, resembling human metabolic syndrome. Previously, we found altered vascular prostanoid (PR) production in this model.
Sodium molybdate (Mo), as well as sodium tungstate, causes insulin‐like effects and normalizes plasma glucose levels in streptozotocin‐treated diabetic rats. We studied the effects of Mo on BP, metabolic parameters and release of PR from the mesenteric vascular bed (MVB) in F‐overloaded rats.
Four groups of male Sprague‐Dawley rats were analysed: Control, tap water to drink; F, F solution 10% W/V to drink; CMo, Mo 100 mg kg day−1 and FMo, both treatments. After 9 weeks, the animals were killed and MVBs removed and the released PRs measured.
F increased BP, glycemia, triglyceridemia and insulinemia. Mo treatment prevented the increases in BP and glycemia, but did not modify triglyceridemia or insulinemia. In addition, Mo decreased BP in controls.
Prostaglandins (PG) F2alpha and E2, PG 6‐ketoF1alpha and thromboxane (TX) B2, as well as inactive metabolites of prostacyclin (PGI2) and TXA2 were detected. F decreased the production of vasodilator PRs PGI2 and PGE2 in MVB. Mo prevented these alterations and increased PGE2 in controls. Vasoconstrict or PRs PGF2alpha and TXA2 release was not modified.
Mo treatment, beyond its known lowering effect on glycemia, prevents the reduction in the vascular release of vasodilator PR observed in this model. This could be one of the mechanisms by which Mo avoids the increase in BP caused by F overload in the rat.</description><identifier>ISSN: 1474-8665</identifier><identifier>EISSN: 1474-8673</identifier><identifier>DOI: 10.1111/aap.12010</identifier><identifier>PMID: 23906370</identifier><language>eng</language><publisher>England: Blackwell Publishing Ltd</publisher><subject>Animals ; Aorta, Thoracic - drug effects ; Aorta, Thoracic - metabolism ; Blood Glucose - drug effects ; Blood Pressure - drug effects ; fructose ; Fructose - adverse effects ; Fructose - antagonists & inhibitors ; hypertension ; Hypertension - metabolism ; Hypertension - prevention & control ; Male ; Mesenteric Arteries - drug effects ; Mesenteric Arteries - metabolism ; metabolic syndrome ; Metabolic Syndrome - chemically induced ; Metabolic Syndrome - metabolism ; Metabolic Syndrome - prevention & control ; molybdate ; Molybdenum - pharmacology ; Prostaglandins - metabolism ; prostanoids ; Rats</subject><ispartof>Autonomic & autacoid pharmacology, 2013-10, Vol.33 (3-4), p.43-48</ispartof><rights>2013 John Wiley & Sons Ltd</rights><rights>2013 John Wiley & Sons Ltd.</rights><rights>Copyright © 2013 John Wiley & Sons Ltd</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3390-a5fba28ccd31220fc7d93794d3fb62aaceb470f5b36f9f703d0982a11bcb4a623</citedby><cites>FETCH-LOGICAL-c3390-a5fba28ccd31220fc7d93794d3fb62aaceb470f5b36f9f703d0982a11bcb4a623</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Faap.12010$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Faap.12010$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,777,781,1412,27905,27906,45555,45556</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23906370$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Peredo, H. A.</creatorcontrib><creatorcontrib>Andrade, V.</creatorcontrib><creatorcontrib>Donoso, A. S.</creatorcontrib><creatorcontrib>Lee, H. J.</creatorcontrib><creatorcontrib>Puyó, A. M.</creatorcontrib><title>Sodium molybdate prevents hypertension and vascular prostanoid imbalance in fructose-overloaded rats</title><title>Autonomic & autacoid pharmacology</title><addtitle>Auton Autacoid Pharmacol</addtitle><description>Summary
Fructose (F) overload produces elevated blood pressure (BP), hyperglycaemia, hypertriglyceridemia and insulin resistance, resembling human metabolic syndrome. Previously, we found altered vascular prostanoid (PR) production in this model.
Sodium molybdate (Mo), as well as sodium tungstate, causes insulin‐like effects and normalizes plasma glucose levels in streptozotocin‐treated diabetic rats. We studied the effects of Mo on BP, metabolic parameters and release of PR from the mesenteric vascular bed (MVB) in F‐overloaded rats.
Four groups of male Sprague‐Dawley rats were analysed: Control, tap water to drink; F, F solution 10% W/V to drink; CMo, Mo 100 mg kg day−1 and FMo, both treatments. After 9 weeks, the animals were killed and MVBs removed and the released PRs measured.
F increased BP, glycemia, triglyceridemia and insulinemia. Mo treatment prevented the increases in BP and glycemia, but did not modify triglyceridemia or insulinemia. In addition, Mo decreased BP in controls.
Prostaglandins (PG) F2alpha and E2, PG 6‐ketoF1alpha and thromboxane (TX) B2, as well as inactive metabolites of prostacyclin (PGI2) and TXA2 were detected. F decreased the production of vasodilator PRs PGI2 and PGE2 in MVB. Mo prevented these alterations and increased PGE2 in controls. Vasoconstrict or PRs PGF2alpha and TXA2 release was not modified.
Mo treatment, beyond its known lowering effect on glycemia, prevents the reduction in the vascular release of vasodilator PR observed in this model. This could be one of the mechanisms by which Mo avoids the increase in BP caused by F overload in the rat.</description><subject>Animals</subject><subject>Aorta, Thoracic - drug effects</subject><subject>Aorta, Thoracic - metabolism</subject><subject>Blood Glucose - drug effects</subject><subject>Blood Pressure - drug effects</subject><subject>fructose</subject><subject>Fructose - adverse effects</subject><subject>Fructose - antagonists & inhibitors</subject><subject>hypertension</subject><subject>Hypertension - metabolism</subject><subject>Hypertension - prevention & control</subject><subject>Male</subject><subject>Mesenteric Arteries - drug effects</subject><subject>Mesenteric Arteries - metabolism</subject><subject>metabolic syndrome</subject><subject>Metabolic Syndrome - chemically induced</subject><subject>Metabolic Syndrome - metabolism</subject><subject>Metabolic Syndrome - prevention & control</subject><subject>molybdate</subject><subject>Molybdenum - pharmacology</subject><subject>Prostaglandins - metabolism</subject><subject>prostanoids</subject><subject>Rats</subject><issn>1474-8665</issn><issn>1474-8673</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkktv1DAUhSNERR-w4A-gSGzaRVo_42Q5GtGBagpIgFhaN_a1cEniwU4G5t_jMu0skJDwxl585-jce1wULym5pPlcAWwuKSOUPClOqFCiamrFnx7etTwuTlO6I4QqLuSz4pjxltRckZPCfgrWz0M5hH7XWZiw3ETc4jil8ttug3HCMfkwljDacgvJzD3EjIQ0wRi8Lf3QQQ-jwdKPpYuzmULCKmwx9gEs2jLClJ4XRw76hC8e7rPiy_Wbz8u31frD6t1ysa4Mz4EqkK4D1hhjOWWMOKNsy1UrLHddzQAMdkIRJzteu9Ypwi1pGwaUdqYTUDN-VpzvfXPAHzOmSQ8-GexzQAxz0lTIRgpBafMfKG9krVp1j77-C70LcxzzIJmqJeNNw0SmLvaUyctJEZ3eRD9A3GlK9H1LOrek_7SU2VcPjnM3oD2Qj7Vk4GoP_PQ97v7tpBeLj4-W1V7h04S_DgqI33X-C0rqr-9X-ua2uZHtcq1X_DdkpquM</recordid><startdate>201310</startdate><enddate>201310</enddate><creator>Peredo, H. A.</creator><creator>Andrade, V.</creator><creator>Donoso, A. S.</creator><creator>Lee, H. J.</creator><creator>Puyó, A. M.</creator><general>Blackwell Publishing Ltd</general><general>Wiley Subscription Services, Inc</general><scope>BSCLL</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>7TK</scope><scope>K9.</scope><scope>7X8</scope></search><sort><creationdate>201310</creationdate><title>Sodium molybdate prevents hypertension and vascular prostanoid imbalance in fructose-overloaded rats</title><author>Peredo, H. A. ; Andrade, V. ; Donoso, A. S. ; Lee, H. J. ; Puyó, A. M.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3390-a5fba28ccd31220fc7d93794d3fb62aaceb470f5b36f9f703d0982a11bcb4a623</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Animals</topic><topic>Aorta, Thoracic - drug effects</topic><topic>Aorta, Thoracic - metabolism</topic><topic>Blood Glucose - drug effects</topic><topic>Blood Pressure - drug effects</topic><topic>fructose</topic><topic>Fructose - adverse effects</topic><topic>Fructose - antagonists & inhibitors</topic><topic>hypertension</topic><topic>Hypertension - metabolism</topic><topic>Hypertension - prevention & control</topic><topic>Male</topic><topic>Mesenteric Arteries - drug effects</topic><topic>Mesenteric Arteries - metabolism</topic><topic>metabolic syndrome</topic><topic>Metabolic Syndrome - chemically induced</topic><topic>Metabolic Syndrome - metabolism</topic><topic>Metabolic Syndrome - prevention & control</topic><topic>molybdate</topic><topic>Molybdenum - pharmacology</topic><topic>Prostaglandins - metabolism</topic><topic>prostanoids</topic><topic>Rats</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Peredo, H. A.</creatorcontrib><creatorcontrib>Andrade, V.</creatorcontrib><creatorcontrib>Donoso, A. S.</creatorcontrib><creatorcontrib>Lee, H. J.</creatorcontrib><creatorcontrib>Puyó, A. M.</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><jtitle>Autonomic & autacoid pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Peredo, H. A.</au><au>Andrade, V.</au><au>Donoso, A. S.</au><au>Lee, H. J.</au><au>Puyó, A. M.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Sodium molybdate prevents hypertension and vascular prostanoid imbalance in fructose-overloaded rats</atitle><jtitle>Autonomic & autacoid pharmacology</jtitle><addtitle>Auton Autacoid Pharmacol</addtitle><date>2013-10</date><risdate>2013</risdate><volume>33</volume><issue>3-4</issue><spage>43</spage><epage>48</epage><pages>43-48</pages><issn>1474-8665</issn><eissn>1474-8673</eissn><abstract>Summary
Fructose (F) overload produces elevated blood pressure (BP), hyperglycaemia, hypertriglyceridemia and insulin resistance, resembling human metabolic syndrome. Previously, we found altered vascular prostanoid (PR) production in this model.
Sodium molybdate (Mo), as well as sodium tungstate, causes insulin‐like effects and normalizes plasma glucose levels in streptozotocin‐treated diabetic rats. We studied the effects of Mo on BP, metabolic parameters and release of PR from the mesenteric vascular bed (MVB) in F‐overloaded rats.
Four groups of male Sprague‐Dawley rats were analysed: Control, tap water to drink; F, F solution 10% W/V to drink; CMo, Mo 100 mg kg day−1 and FMo, both treatments. After 9 weeks, the animals were killed and MVBs removed and the released PRs measured.
F increased BP, glycemia, triglyceridemia and insulinemia. Mo treatment prevented the increases in BP and glycemia, but did not modify triglyceridemia or insulinemia. In addition, Mo decreased BP in controls.
Prostaglandins (PG) F2alpha and E2, PG 6‐ketoF1alpha and thromboxane (TX) B2, as well as inactive metabolites of prostacyclin (PGI2) and TXA2 were detected. F decreased the production of vasodilator PRs PGI2 and PGE2 in MVB. Mo prevented these alterations and increased PGE2 in controls. Vasoconstrict or PRs PGF2alpha and TXA2 release was not modified.
Mo treatment, beyond its known lowering effect on glycemia, prevents the reduction in the vascular release of vasodilator PR observed in this model. This could be one of the mechanisms by which Mo avoids the increase in BP caused by F overload in the rat.</abstract><cop>England</cop><pub>Blackwell Publishing Ltd</pub><pmid>23906370</pmid><doi>10.1111/aap.12010</doi><tpages>6</tpages></addata></record> |
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| subjects | Animals Aorta, Thoracic - drug effects Aorta, Thoracic - metabolism Blood Glucose - drug effects Blood Pressure - drug effects fructose Fructose - adverse effects Fructose - antagonists & inhibitors hypertension Hypertension - metabolism Hypertension - prevention & control Male Mesenteric Arteries - drug effects Mesenteric Arteries - metabolism metabolic syndrome Metabolic Syndrome - chemically induced Metabolic Syndrome - metabolism Metabolic Syndrome - prevention & control molybdate Molybdenum - pharmacology Prostaglandins - metabolism prostanoids Rats |
| title | Sodium molybdate prevents hypertension and vascular prostanoid imbalance in fructose-overloaded rats |
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