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目的 :探讨低氧对大鼠心脏钠尿肽C受体 (NPR C)表达的调节作用 ,以及血管钠肽 (VNP)对这一过程的影响。方法 :将大鼠随机分为 3组 :对照组、低氧组 (3～ 2 8d)和VNP(2 5～ 75 μg/kgbw) +低氧组 ,采用放射免疫的方法测定大鼠血浆心房钠尿肽 (ANP)的浓度 ,并采用定量PCR的方法分析NPR C的mRNA水平。结果 :低氧 2 8d大鼠血浆ANP浓度显著高于正常大鼠 (P <0 .0 5 ) ,而且每天注射 75 μg/kgbw的VNP使ANP浓度进一步升高 (P <0 .0 1)。低氧 3d对大鼠心脏NPR C的mRNA的量没有显著影响 ;低氧 7d使大鼠心脏NPR C的mRNA的拷贝数显著升高 (P <0 .0 5 ) ;低氧 14d、2 8d使大鼠心脏NPR C的mRNA的拷贝数进一步升高 (P <0 .0 1)。每日注射 2 5μg/kgbw的VNP对低氧诱导的大鼠心脏NPR C表达没有显著影响 ;5 0 μg/kgbw的VNP显著降低低氧大鼠心脏NPR C的表达 (P <0 .0 5 ) ;75 μg/kgbw的VNP进一步降低低氧大鼠心脏NPR C的表达 (P <0 .0 1)。 结论 :VNP可以升高低氧大鼠的血浆ANP水平 ;低氧可以使大鼠心脏NPR C表达增加 ,而且具有时间依赖性 ,而VNP对这一过程有抑制作用 ,并且呈剂量依赖性
AIM: To investigate the regulatory effect of hypoxia on the expression of NPR C and the effect of vascular sodium peptide (VNP) on this process. Methods: The rats were randomly divided into 3 groups: control group, hypoxia group (3 ~ 28 days) and VNP (25 ~ 75 μg / kg bw) + hypoxia group. Radioimmunoassay was used to determine plasma atrial natriuretic peptide Urine peptide (ANP) was assayed and NPR C mRNA levels were analyzed by quantitative PCR. Results: The ANP concentration in hypoxia 28 d rats was significantly higher than that in normal rats (P <0.05), and the daily injection of 75 μg / kg bw VNP increased the ANP concentration (P <0.01). Hypoxia 3d had no significant effect on the amount of NPR C mRNA in rat hearts; hypoxia 7d increased NPR C mRNA copy number significantly (P <0.05); hypoxia 14d and 28d The rat heart NPR C mRNA copy number increased further (P <0.01). The daily injection of VNP at 25μg / kgbw had no significant effect on the expression of NPR C in hypoxia-induced rat hearts; VNP at 50 μg / kgbw significantly reduced the expression of NPRC in hypoxic rat hearts (P <0.05) ; VNP at 75 μg / kgbw further reduced NPR C expression in hypoxic rat hearts (P <0.01). Conclusion: VNP can increase the plasma ANP level in hypoxic rats. Hypoxia can increase the expression of NPR C in rat heart in a time-dependent manner, while VNP can inhibit this process in a dose-dependent manner