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孕期自发性高血压鼠服卡托普利预防子鼠高血压及其机制 |
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初少莉 马燕红 赵光胜
摘要 目的：探讨自发性高血压大鼠(SHR)在孕期服转换酶抑制剂卡托普利预防子鼠高血压的作用及其肾素血管紧张素系统机制。方法：观察孕期服卡托普利(Cap 100 mg.kg-1.d-1)对子鼠收缩压的影响；以放免法和反转录-聚合酶链式反应法分别测血浆、组织血管紧张素Ⅱ(AngⅡ)浓度和组织AngⅡ-Ⅰ型受体(AT1)mRNA表达。结果：SHR单纯在孕期服用卡托普利能有效拮抗子鼠随增龄的升压幅度(P＜0.01)；同时降低其大脑皮质、肾皮质AngⅡ浓度，增高AT1mRNA表达。结论：证实胚胎期是SHR发病的关键阶段，在此期干扰AngⅡ的生成能有效预防子鼠发生高血压，为高血压病的防治提供了实验性启示。
主题词 高血压；大鼠；卡托普利；血管紧张素Ⅱ；受体，血管紧张素
Prevention of genetic hypertension and its mechanisms in
descendants of SHRs by captopril treatment during pregnancy
CHU Shao-Li,MA Yan-Hong,ZHAO Guang-Sheng
Rui Jin Hospital Affiliated to Shanghai Second Medical University,Shanghai Institute of Hypertension,Shanghai(200025)
Abstracts AIM and METHODS：To explore the prevention effect of hypertension and its renin-angiotensin system mechanism in descendants of SHRs (spontaneously hypertensive rate) by 100 mg/kg.d-1 captopril,angiotensin converting enzyme inhibitor,intervention during pregnancy,the systolic blood pressure,plasma and tissue angiotensin(AngⅡ),detected by radio-immunoassay,and tissue AngⅡ-Ⅰ type receptor(AT1) mRNA expression by reverse transcription-polymerase chain reaction method. RESULTS：Captopril intervention during pregnancy can effectively prevent the increment of blood pressure by age (P＜0.01) in descendant SHRs; and decrease its AngⅡ concentrations in cerebral cortex,while AT1 mRNA expression increased. CONCLUSIONS：It is confirmed that the embryo stage might be the critical period for the development of hypertension in SHR,and the interference of AngⅡ production could effectively prevent the occurrence of hypertension in descendant SHRs thus offering an experimental clue for the prevention and control of essential hypertension.
MeSH Hypertension; Rats; Captopril; Angiotensin Ⅱ; Receptors,angiotensin
肾素-血管紧张素系统(renin-angiotensin system,RAS)系血压的重要调节因子，其主要活性物质血管紧张素Ⅱ(angiotensin Ⅱ，AngⅡ)是很强的缩血管和促细胞生长因子，可能参与高血压病(essential hypertension,EHT)的发生与维持。ATⅡ-Ⅰ型受体([1] [2] 下一页
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