摘要
目的 探讨ACEI或ATⅡRA对肾脏的保护作用 ,证实是否存在肾脏水平的醛固酮逃逸。 方法 以高血压鼠 (SHR)为研究对象 ,观察血管紧张素转换酶抑制剂 (ACEI)依那普利、培哚普利及血管紧张素Ⅱ受体 1拮抗剂 (ATⅡRA)氯沙坦长期治疗高血压对肾脏局部醛固酮合成的影响。用肾脏离体灌注 ,反向高效液相分离纯化和放免检测肾脏局部合成的醛固酮 ,逆转录 聚合酶链反应 (RT PCR)证实对肾脏表达醛固酮合成酶基因CYP11B2mRNA的作用。 结果 治疗 5月后依那普利、培哚普利以及氯沙坦均明显降低SHR肾脏合成醛固酮及CYP11B2mRNA的表达 ,其中培哚普利可抑制其合成至正常水平。 结论 长期ACEI或ATⅡRA治疗持久地抑制肾脏局部醛固酮的合成 ,提示不存在肾脏水平的醛固酮逃逸。
Objective To investigate the effects of long-term ACEI or AT ⅡRA therapy on aldosterone produced in spontaneously hypertensive rat(SHR) kidneys and to investigate whether aldosterone escape occurs in kidneys or not. Methods By means of ex vivo kidney perfusion,high performance liquid chromatography(HPLC) and radioimmunoassay(RIA),aldosterone produced in kidneys was measured.Expression of aldosterone synthase gene CYP11B2 mRNA in the kidneys was determined by RT-PCR. Results Compared with those of the untreated SHR group,the levels of aldosterone and CYP11B2 mRNA expression in the rats treated with enalapril,perindopril and losartan for five months were significantly lower( P<0.05,P<0.01 respectively).Perindopril most inhibited aldosterone production,and the level couldn't reach the normal levels. Conclusions Long-term ACEI and AT ⅡRA treatment significantly inhibited the aldosterone production in kidneys that indicated aldosterone escape phenomenon did not occur in kidneys.
出处
《实用老年医学》
CAS
2004年第2期75-77,共3页
Practical Geriatrics
