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(18μg/d)14d;环孢素A组皮下注射Ald(18μg/d),环孢素A(5mg·g-1·d-1)皮下注射14d。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。
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.
出处
《心脏杂志》
CAS
2005年第2期109-110,114,共3页
Chinese Heart Journal
基金
十五军队重点基金资助(No.02Z0010)
关键词
醛固酮
神经肽Y
信号通路
aldosterone
neuropeptide Y
signal-pathway
