醛固酮上调大鼠组织钙调神经磷酸酶活性及抑制血浆一氧化氮水平

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目的 研究醛固酮对大鼠重要脏器心、脑、肾、脾、肺和肝脏中钙调神经磷酸酶(CaN)活性及血浆血管紧张素Ⅱ(AngⅡ)、内皮素(ET-1)和一氧化氮(NO)水平的影响,探讨醛固酮在CaN依赖的信号传导通路中的作用。方法 取21只雄性Wistar大鼠随机分为3组:醛固酮(Ald)组(腹腔内注射Ald 18μg/d 4周)、环孢霉素A(CsA)干预组(以Ald处理同时腹腔内给予CsA 5mg/kg·d注射共4周)及正常对照组。采用放免法测定血浆AngⅡ、Ald和ET-1浓度,采用比色测定NO浓度及大鼠各组织器官CaN活性。结果 Ald组大鼠血浆NO_3~-浓度较对照组明显下降(P<0.05),CsA干预后血NO_3~-浓度明显回升(P<0.05)。各组AngⅡ、ET-1浓度无明显变化。Ald组大鼠心、脾、肾、肺、脑和肝脏中CaN活性较正常对照组分别上升147%、65%、38%、100%、43%和50%(均P<0.05),CsA干预显著缓解上述组织器官CaN活性的上升(P<0.05)。结论 醛固酮能上调大鼠重要组织脏器CaN活性并抑制血浆NO水平,可能在激活CaN依赖的信号传导通路中具有重要作用。 Objective To investigate the effects of aldosterone on the activity of calcineurin (CaN) and the levels of plasma angiotensin Ⅱ (AngⅡ), endothelin (ET-1) and nitric oxide synthase in heart, brain, kidney, Nitrogen (NO) levels of the role of aldosterone in CaN-dependent signaling pathway. Methods Twenty-one male Wistar rats were randomly divided into three groups: aldosterone (Ald) group (intraperitoneal injection of Ald 18 μg / d for 4 weeks) and cyclosporine A (CsA) intervention group 5mg / kg · d injection for 4 weeks) and normal control group. Plasma concentrations of AngⅡ, Ald, and ET-1 were measured by radioimmunoassay. NO concentrations were measured by colorimetric assay and CaN activity in various tissues and organs of rats. Results The concentration of NO 3 - in plasma of rats in Ald group was significantly lower than that in control group (P <0.05). After the intervention of CsA, the concentration of NO 3 - in blood increased significantly (P <0.05). The concentration of AngⅡ and ET-1 in each group had no significant change. The activity of CaN in heart, spleen, kidney, lung, brain and liver in Ald group increased by 147%, 65%, 38%, 100%, 43% and 50% respectively compared with the normal control group (all P <0.05) Significantly alleviate the above tissue and organ CaN activity (P lt; 0.05). Conclusion Aldosterone can up-regulate the activity of CaN in vital organs of rats and inhibit the level of NO in plasma, which may play an important role in the activation of CaN-dependent signal transduction pathway.
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