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外源性醛固酮负性调控大鼠血浆神经肽Y的相关信号通路(PDF)

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2005年第2期
页码:
109-110,114
栏目:
基础研究
出版日期:
2005-03-05

文章信息/Info

Title:
The correlated signalpathway in ectogenesis aldosterone negatively control neuropeptide Y in rats
作者:
李朝晖; 谢晓华; 刘丽; 常连庆; 陈雯; 邓朝阳
解放军总医院南四科， 北京 100853
Author(s):
LI Zhaohui;  XIE Xiaohua;  LIU Li;  CHANG Lianqing;  CHEN Wen;  DENG Zhaoyang
General Hospital of PLA, Beijing, 100853, China
关键词:
醛固酮; 神经肽Y; 信号通路
Keywords:
aldosterone; neuropeptide Y; signalpathway
分类号:
R543
DOI:
-
文献标识码:
A
摘要:
目的 探讨醛固酮(Ald)诱导心肌肥大的大鼠模型中，负性调控血浆神经肽Y(NPY)所涉及的信号转导机制。方法 健康雄性Wistar大鼠，随机分为3组：正常对照组；Ald组：皮下注射Ald (18 μg/d) 14 d；环孢素A组：皮下注射Ald(18 μg/d)，环孢素A (5 mg·g-1·d-1)皮下注射14 d。测量尾动脉压，取心脏测量左心室质量/体质量（LVW/BW），用放免方法测定血浆NPY、血管紧张素Ⅱ（AⅡ）、Ald含量。结果 Ald组较正常组LVW/BW升高，NPY和AⅡ下降，Ald增加；环孢素A组较醛固酮组LVW/BW降低，NPY、AⅡ和Ald增加。结论 外源性醛固酮可通过激活钙调神经磷酸酶信号通路，负性调控大鼠神经肽Y的生成和分泌。
Abstract:
AIM To investigate the mechanism of ectogenesis aldosterone(Ald) negatively control neuropeptide Y(NPY) level in plasma, in Aldinduced cardiac hypertrophy rats. METHODS Male Wistar rats were randomly divided into three groups: control group, Ald group treated with Ald (18 μg/d 14 d), and cyclosporin A group treated with Ald (18 μg/d ×14 d) and cyclosporin A (5 mg·g-1·d-1 ×14 d). The NPY、AⅡ and Ald level in plasma were determined by radioimmunoassay. RESULTS The NPY and AⅡ level decreased , and Ald level increased in aldosterone group compared with control group. But NPY level markedly increased in cyclosporin A group compared with Ald group. CONCLUSION Ectogenesis Ald can negatively control the generation and secretion of NPY, through calcineurin depended signalpathway.

参考文献/References

［1］ Onuoha GN, Nicholls DP, Alpar EK, et al. Regulatory peptides in the heart and major vessels of man and mammals ［J］. Neuropeptides,1999, 33 (2): 165-172.

［2］刘润梅，张志寿，佟万仁. 神经肽Y与冠心病的关系［J］. 心脏杂志, 2000, 12(4):314-315.

［3］李朝晖, 谢晓华, 刘 丽, 等. 醛固酮对大鼠血浆神经肽Y的影响［J］. 心脏杂志，2004，16（3）：221－225.

备注/Memo

备注/Memo:
收稿日期：2004-08-19.基金项目: 十五军队重点基金资助(No. 02Z0010)
更新日期/Last Update: 2010-01-05