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目的：在阿霉素诱导的肾病综合征大鼠动物模型探讨肾病水肿发病机理。方法：观察阿霉素诱导的肾病综合征大鼠模型扩容利尿反应及心钠素（ＡＮＰ）两种受体的表达。结果：肾病大鼠对扩容利尿的反应较正常对照组明显下降（Ｐ＜０．０１）。虽然两组大鼠在扩容时血浆心钠素上升幅度相似，但其尿中ＡＮＰ第二信使ｃＧＭＰ的排泄（ＵｃＧＭＰＶ）在肾病组比正常对照组明显下降（５．８５±２．６～３１．４±７．５ｖｓ６．０２±３．０～９８．４５±１６．８ｐｍｏｌ／ｍｉｎ，Ｐ＜０．０１）。Ｎｏｒｔｈｅｒｎ杂交显示，两组大鼠肾脏ＡＮＰ－Ａ受体ｍＲＮＡ表达相似，但肾病组大鼠肾脏ＡＮＰ－Ｃ受体ｍＲＮＡ表达较正常对照组明显升高（Ａ×ａｒｅａ１ｖｓ０．３２，Ｐ＜０．０１）。结论：肾病综合征水钠潴留可能与其肾脏ＡＮＰ－Ｃ受体高表达有关。
Objective: To investigate the pathogenesis of nephrotic edema in animal model of adriamycin-induced nephrotic syndrome. Methods: To observe the dilatation and diuretic response and the expression of atrial natriuretic peptide (ANP) receptors in doxorubicin-induced nephrotic syndrome rat model. Results: The response of nephrotic rats to dilatation of diuresis was significantly lower than that of normal control group (P <0.01). Although plasma atrial natriuretic peptide increased similarly in both groups, urinary excretion of urinary cGMP excretion (UcGMPV) decreased significantly in nephropathy group compared with normal control group (5.85 ± 2.6-31). 4 ± 7.5 vs 6.02 ± 3.0 to 98.45 ± 16.8 pmol / min, P <0.01). Northern blot showed that ANP-A mRNA expression was similar in both groups, but the renal ANP-C receptor mRNA expression in renal disease group was significantly higher than that in normal control group (A × area1vs0.32, P <0.01) ). Conclusion: Nephrotic syndrome Shuinazhuliu may be related to its high renal ANP-C receptor expression.