【摘要】 目的：从肾素血管紧张素系统(RAS)角度初步探讨在肾素依赖性高血压大鼠(RHR)中胰岛素抵抗(IR)与高血压左室肥厚(LVH)的关系,以及血管紧张素Ⅱ(AngⅡ)受体拮抗剂氯沙坦(Losartan)对IR和LVH的逆转作用。方法：Wistar雄性大鼠50只,按Kuwajima法制成两肾—夹肾性高血压模型后,随机分为A、B、C 3组,A组为对照组,普通饲料喂养。B组为高糖组,高蔗糖饲料喂养,C组为氯沙坦组,高蔗糖饲料喂养的同时给予氯沙坦。3周、8周观察其空腹血糖(FPG)、空腹胰岛素(FINS)的水平,8周时测其血浆和心肌组织的肾素、AngⅡ、醛固酮(AID)水平,以及左室相对质量(LVW／BW)。结果：不同饲料喂养后,氯沙坦组8周时FINS水平和胰岛素敏感指数与其3周时相比,无显著性差异(P＞0.05),与8周时高糖组和对照组相比,差异有显著性(P＜0.05)。8周时高糖组血浆肾素、AngⅡ水平与对照组相比无显著性(P＞0.05),血浆ALD水平较对照组增加28％,有显著性(P＜0.05)；心肌组织中肾素、AngⅡ、ALD水平与对照组相比分别增加20％、30％、23％,具有显著性(P＜0.01),氯沙坦组血浆和心肌组织的肾素、AngⅡ水平与高糖组和对照组相比明显升高,差异有显著性(P＜0.05),氯沙坦组血浆和心肌组织的ALD水平则明显降低,与高糖组相比,差异有显著性(P＜0.05)。高糖组LVW／BW与对照组和氯沙坦组相比明显增加,差异具有显著性(P＜0.05),而氯沙坦组LVW／BW与对照组相比,差异无显著性(P＞0.05)。结论：IR促进RHR LVH的形成,可能与高胰岛素血症引起心肌组织RAS的激活有关；氯沙坦可以改善IR和逆转LVH。更多还原

【Abstract】 Objective: From the point of view of renin - angiotensin system（RAS）, to investigate the correlation of insulin resistance and left ventricular hypertrophy （LVH） in renal hypertensive rats （RHR）, and insulin resistance and LVH were reversed by angiotensin Ⅱ AT₁ receptor antagonist losartan. Methods: According to Kuwajima method, 50 male Wistar rats were producd renal hypertension model by two kidney one clip. All rats were divided into A, B, C groups randomly. Group A was fed with standard chew, group B was fed with high sucrose, group C was fed with high sucrose and losartan. After 3 weeks and 8 weeks, levels of fasting plasma glucose and fasting plasma insulin were tested;and After 8 weeks, renin - angiotensin Ⅱ - aldosterone in plasma and myocardium tissue and left ventricular weight/body weight （LVW/BW） were tested.Results: The levels of fasting plasma insulin and insulin sensitive index in losartan group had no significant difference compared with 3 weeks and 8 weeks（P＞0.05）, but had significant difference compared with control group and sucrose, group（P＜0.05）. At 8rd weeks, while little difference of plasma rennin and angiotensin Ⅱ were found between group A and group B （P＞0.05）, plasma aldosterone increased 28% in group B （P＜0.05）, Renin, angiotensin Ⅱ and aldosterone in myocardium tissue were increased 20%, 30% and 23% respectively in group B （P＜0.01）. At Iosartan group, the levels of renin and Angiotensin Ⅱ in plasm and myocardium tissue were increased compared with sucrose group and control group（P＜0.05）, the levels of aldosterone in plasm and myocardium tissue were decreased compared with sucrose group（ P＜0.01）. LVW/BW in sucrose group was increased compared with control group and Losartan group （P＜0.05）, but in losartan group, LVW/BW had no significant difference compared with control group（P＞0.05）. Conclusion: Insulin resistance facilitated left ventricular hypertrophy in renin hypertensive rats. Hyperinsulinism may initiate activation of RAS in myocardium tissue. Angiotensin Ⅱ AT₁ receptor antagonist losartan might improved insulin resistance and reversed left ventricular hypertrophy.更多还原