卡托普利调节早期糖尿病大鼠肾脏诱生型一氧化氮合成酶基因表达

Captoprilregulatingrenalinduciblenitricoxidesynthaseexpressioninearlydiabeticrats

应用廓清实验和逆转录半定量聚合酶链式反应（ＰＣＲ）分析研究了卡托普利（ｃａｐｔｏｐｒｉｌ）对糖尿病早期肾血液动力学的影响及其机制。结果卡托普利可纠正４周糖尿病大鼠的肾脏高灌注、高滤过；半定量ＰＣＲ分析显示非卡托普利治疗的４周糖尿病大鼠肾脏皮、髓质诱生型一氧化氮合成酶（ｉＮＯＳ）基因表达显著上调，而卡托普利治疗鼠肾脏皮、髓质ｉＮＯＳｍＲＮＡ水平明显低于非治疗鼠。结论抑制过高的ＮＯ产生可能是卡托普利影响糖尿病早期肾血液动力学的机制之一。

bjectiveToinvestigatethatwhethernitricoxide(NO)playsaroleonregulatingabnormaldiabeticrenalhemodynamics.MethodsThemechanismunderlyingcaptoprilafectingearlydiabeticrenalhemodynamicswasin┐vestigated.ResultsClearancestudyshowedthatcaptoprilcouldcorrectelevatedrenalplasmaflow(RPF,3.61±0.27vs4.54±0.24ml·min-1/100gwt,P<0.05)andglomerularfiltratingrates.(GFR1.03±0.03vs1.15±0.04ml·min-1/100gwt,P<0.05)inearlydiabeticrats.Reversetranscription,semi-quantitativePCRanalysisshowedthatearlydiabeticrenalcorticalandmedularyinduciblenitricoxidesynthase(iNOS)geneexpressionrosesignificantly(P<0.01),captopriltreatmentmadeiNOSmRNAlevellowermarkedly(P<0.01).ConclusionInhibitionofover-expressednitricoxide(NO)productionindiabeticratkidneymayplayanimportantroleforthebeneficialefectofcaptoprilonregulatingabnormaldiabeticrenalhemodynamics.