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首页> 外文期刊>High Altitude Medicine & Biology >Upregulation of Arginase Expression and Activity in Hypertensive Rats Exposed to Chronic Intermittent Hypobaric Hypoxia
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Upregulation of Arginase Expression and Activity in Hypertensive Rats Exposed to Chronic Intermittent Hypobaric Hypoxia

机译:慢性间歇性低压低氧对高血压大鼠精氨酸酶表达和活性的上调

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Lopez, Vasthi, Patricia Siques, Julio BritCarmen Vallejos, Nelson Naveas, Claudia Carvallo, Fabiola Leo ´n-nVelarde, and Nelson Carvajal. Upregulation of arginase expression and activity in hypertensive rats exposed tonchronic intermittent hypobaric hypoxia. High Alt. Med. Biol. 10:373–381, 2009.— The aim of this study was tonanalyze the activity and expression levels of arginase I and II and to monitor the cardiovascular and hemato-nlogical responses in tolerant and intolerant rats exposed to chronic intermittent hypobaric hypoxia (CIHH). MalenWistar rats (age: 3.0u00010.4 months, weight: 250u000125 g; n¼30) were randomly divided into two groups: CIHH2u00022n(2 days hypoxia, 2 days normoxia, n¼20) and NX (normoxia, n¼10). The hypoxia was simulated in a hypobaricnchamber at 428 torr. Tolerance was determined according to a previous protocol. Arginase activity was measurednin lung and heart tissues, and the expression levels were determined by a (RT-PCR) assay in lung tissue. Resultsnshowed that the intolerants rats had lower body weight, higher hematocrit (Hct) (74u00014% vs. 61u00012%, p<0.05),nhigher values of systolic blood pressure (SBP) (183u00013.7 mmHg vs. 147u00015.4 mmHg, p<0.05), and higher ar-nginase activity. In addition, RT-PCR analysis from lung tissue showed an overexpression of arginase II in thenintolerant group ( p<0.01). However, tolerants had similar values as the NX group ( p¼ns). Further, a correlationnwas found between arginase activity and SBP in the heart (rn2n¼0.596, p<0.001). An upregulation of arginase typenII could be pivotal in understanding the pathogenesis of systolic hypertension and probably other phenomenanassociated with intermittent hypobaric hypoxia. A schematic explanation of these relations is proposed.
机译:洛佩兹(Lopez),瓦西(Vasthi),帕特里夏·西克斯(Patricia Siques),朱利奥·布里特·卡门·瓦列霍斯(Julio BritCarmen Vallejos),纳尔逊·纳维斯(Nelson Naveas),克劳迪娅·卡瓦洛(Claudia Carvallo),法比奥拉·莱奥·n·韦拉德(Fabiola Leo n-nVelarde)和纳尔逊·卡瓦哈尔(Nelson Carvajal)。高血压大鼠暴露于tonchronic间歇性低压氧不足时,精氨酸酶表达和活性上调。高Alt。中生物学10:373–381,2009年。这项研究的目的是分析精氨酸酶I和II的活性和表达水平,并监测暴露于慢性间歇性低压缺氧(CIHH)的耐受性和不耐受性大鼠的心血管和血液学反应。将雄性Wistar大鼠(年龄:3.0u00010.4个月,体重:250u000125 g;n¼30)随机分为两组:CIHH2u00022n(缺氧2天,常氧2天,n¼20)和NX(常氧,n¼10)。在428托的低压舱中模拟了缺氧。公差是根据先前的方案确定的。在肺和心脏组织中测量精氨酸酶活性,并通过(RT-PCR)测定法在肺组织中测定表达水平。结果表明,不耐受的大鼠体重较低,血细胞比容(Hct)较高(74u00014%对61u00012%,p <0.05),收缩压(SBP)值较高(183u00013.7 mmHg对147u00015.4 mmHg,p <0.05)和更高的精氨酸酶活性。此外,肺组织的RT-PCR分析表明,耐高脂组中精氨酸酶II的过表达(p <0.01)。但是,宽容度与NX组(p¼ns)相似。此外,在心脏中发现了精氨酸酶活性与SBP之间的相关性(rn2n¼0.596,p <0.001)。 Ⅱ型精氨酸酶的上调对于理解收缩期高血压的发病机制以及可能与间歇性低压缺氧有关的其他现象至关重要。提出了这些关系的示意图。

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