醛固酮促进血管紧张素Ⅱ诱导大鼠心脏成纤维细胞合成胶原
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湖北省教育厅资助课题(2002X00003)


Aldosterone Potentiate AngiotensinⅡ-Induced Collagen Synthesis in Rat Cardiac Fibroblasts
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    摘要:

    为探讨醛固酮对大鼠心脏成纤维细胞血管紧张素Ⅱ1型受体表达的影响及醛固酮对血管紧张素Ⅱ促进心脏成纤维细胞胶原代谢效应的影响,采用3 H 脯氨酸掺入法对体外分离培养的心脏成纤维细胞分别检测醛固酮、血管紧张素Ⅱ以及二者共同作用后对心脏成纤维细胞胶原合成量的影响;分别利用放射配体结合实验和半定量逆转录—聚合酶链反应测定经醛固酮处理后细胞血管紧张素Ⅱ 1型受体及其mRNA的表达水平,并比较其与对照组间的差异。结果发现血管紧张素Ⅱ(10 -7mol/L)可使心脏成纤维细胞胶原合成量显著增加(P<0 .0 1) ,醛固酮对心脏成纤维细胞的胶原合成无影响,但醛固酮可明显地增强血管紧张素Ⅱ促进心脏成纤维细胞胶原合成的效应;经醛固酮(10 -7mol/L)处理的心脏成纤维细胞血管紧张素Ⅱ 1型受体的表达与对照组比较明显升高(2倍) ,细胞血管紧张素Ⅱ1型受体mRNA的水平也较对照组显著增加(1.5倍)。结果说明醛固酮虽然不能通过直接作用影响心脏成纤维细胞的胶原代谢,但它可以通过上调心脏成纤维细胞血管紧张素Ⅱ 1型受体的表达来增强血管紧张素Ⅱ致心脏成纤维细胞胶原合成增多的效应

    Abstract:

    Aim To investigate the effect of aldosterone on expression of angiotensin Ⅱ type 1 (AT1) receptor in rat cardiac fibroblasts (CFs) and test the effect of aldosterone on AngⅡ induced collagen synthesis. Methods Cardiac fibroblasts culture were established from neonatal rats. Collagen synthesis was measured by 3 H proline incorporation after incubation with AngⅡ, aldosterone and AngⅡ plus aldosterone. The density of AT 1 recetpor was determined by 125 Ⅰ Ang Ⅱ saturation binding, and AT1 receptor mRNA levels were analyzed by quantitative reverse transcriptase polymerase chain reaction(RT PCR). Results AngⅡ increased collagen synthesis in cultured CFs; while aldosterone did not affect production of collagen. However, aldosterone could significantly potentiate the incremental effect of AngⅡ on collagen synthesis in CFs. The density of AT1 receptor inceased 2 fold and was accompanied by a 1.5 fold increase in the corresponding mRNA after treatment of aldosterone(10 -7 mol/L). Conclusion Aldosterone does not exert a direct effect on collagen synthesis in cultured rat CFs, but could influence the collagen output of CFs through the upregulated AT1 receptor.

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曹政,王家宁,杨桂元,李建军.醛固酮促进血管紧张素Ⅱ诱导大鼠心脏成纤维细胞合成胶原[J].中国动脉硬化杂志,2003,11(2):135~138.

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  • 收稿日期:2002-10-22
  • 最后修改日期:2003-03-05
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