H. A. Peredo, V. Andrade, A. S. Donoso, H. J. Lee, A. M. Puyó
{"title":"钼酸钠对果糖超载大鼠高血压和血管前列腺素失衡的预防作用","authors":"H. A. Peredo, V. Andrade, A. S. Donoso, H. J. Lee, A. M. Puyó","doi":"10.1111/aap.12010","DOIUrl":null,"url":null,"abstract":"<div>\n \n <p>\n \n </p><ol>\n \n <li>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.</li>\n \n <li>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.</li>\n \n <li>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<sup>−1</sup> and FMo, both treatments. After 9 weeks, the animals were killed and MVBs removed and the released PRs measured.</li>\n \n <li>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.</li>\n \n <li>Prostaglandins (PG) F<sub>2</sub>alpha and E<sub>2,</sub> PG 6-ketoF<sub>1</sub>alpha and thromboxane (TX) B<sub>2</sub>, as well as inactive metabolites of prostacyclin (PGI<sub>2</sub>) and TXA<sub>2</sub> were detected. F decreased the production of vasodilator PRs PGI<sub>2</sub> and PGE<sub>2</sub> in MVB. Mo prevented these alterations and increased PGE<sub>2</sub> in controls. Vasoconstrict or PRs PGF<sub>2</sub>alpha and TXA<sub>2</sub> release was not modified.</li>\n \n <li>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.</li>\n </ol>\n \n </div>","PeriodicalId":100151,"journal":{"name":"Autonomic and Autacoid Pharmacology","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2013-08-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/aap.12010","citationCount":"8","resultStr":"{\"title\":\"Sodium molybdate prevents hypertension and vascular prostanoid imbalance in fructose-overloaded rats\",\"authors\":\"H. A. Peredo, V. Andrade, A. S. Donoso, H. J. Lee, A. M. Puyó\",\"doi\":\"10.1111/aap.12010\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div>\\n \\n <p>\\n \\n </p><ol>\\n \\n <li>Fructose (F) overload produces elevated blood pressure (BP), hyperglycaemia, hypertriglyceridemia and insulin resistance, resembling human metabolic syndrome. 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引用次数: 8
摘要
果糖(F)过量会导致血压升高、高血糖、高甘油三酯血症和胰岛素抵抗，类似于人类代谢综合征。在此之前，我们在该模型中发现了血管前列腺素(PR)生成的改变。钼酸钠(Mo)和钨酸钠在链脲佐菌素治疗的糖尿病大鼠中引起胰岛素样作用并使血浆葡萄糖水平正常化。我们研究了Mo对f -超载大鼠血压、代谢参数和肠系膜血管床(MVB) PR释放的影响。对四组雄性sd大鼠进行了分析:对照组，饮用自来水;F、F溶液10% W/V饮用;CMo, Mo 100 mg kg day - 1和FMo，两种处理。9周后，杀死动物，移除MVBs，测量释放pr。F升高血压、血糖、甘油三酯血症和胰岛素血症。没有治疗阻止血压和血糖升高，但没有改变甘油三酯血症或胰岛素血症。此外，Mo降低了对照组的血压。检测前列腺素(PG) f2 α和E2, PG 6-酮f1 α和血栓素(TX) B2，以及前列腺素(PGI2)和TXA2的无活性代谢物。F降低MVB血管扩张剂pr、PGI2和PGE2的产生。Mo阻止了这些改变，并增加了对照组的PGE2。血管收缩或PRs PGF2alpha和TXA2的释放没有改变。除了已知的降血糖作用外，在该模型中观察到，没有任何治疗可以阻止血管扩张剂PR的血管释放减少。这可能是Mo避免大鼠体内F超载引起的血压升高的机制之一。
Sodium molybdate prevents hypertension and vascular prostanoid imbalance in fructose-overloaded rats
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.
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