首页> 外文期刊>International heart journal >Effects of ARB or ACE-inhibitor administration on plasma levels of aldosterone and adiponectin in hypertension.
【24h】

Effects of ARB or ACE-inhibitor administration on plasma levels of aldosterone and adiponectin in hypertension.

机译:ARB或ACE抑制剂对高血压患者血浆醛固酮和脂联素水平的影响。

获取原文
获取原文并翻译 | 示例
           

摘要

Aldosterone production causes vascular injury and may occur despite the long-term administration of angiotensin converting enzyme-inhibitors (ACE-I) (ie, aldosterone breakthrough). The angiotensin II receptor blocker (ARB) telmisartan can function as a ligand for peroxisome proliferator-activated receptor (PPAR) gamma. Stimulation of PPAR gamma has been demonstrated to raise adiponectin production and suppress angiotensin II type 1 receptor expression. Thus, we investigated the effect of the ACE-I perindopril erbumin (perindopril) and the ARB telmisartan on plasma levels of aldosterone and adiponectin.Patients with essential hypertension were randomly assigned to receive 48 weeks of perindopril (2-8 mg/d) or telmisartan (20-80 mg/d). We measured adiponectin, aldosterone, angiotensin II, and renin at weeks 0, 8, 24, and 48.A total of 53 subjects were randomized. Data on 51 subjects (25 in the perindopril group and 26 in the telmisartan group; mean age, 65.1 years) were available for analyses. Plasma aldosterone decreased significantly in both the telmisartan (69.9+/-5.6 to 58.1+/-5.4 pg/mL) and perindopril (74.1+/-4.7 to 64.7+/-5.3 pg/mL) groups at 8 weeks, but returned toward the baseline in the perindopril group (67.9+/-4.1 pg/mL) at 24 weeks. Plasma glycated hemoglobin levels or urine albumin did not change significantly after the treatment in either group.Telmisartan seemed to be more effective at suppressing aldosterone and raising adiponectin levels than perindopril; however, improvements in insulin sensitivity and albuminuria were not detected. These results are consistent with the idea that the use of an ARB with PPAR gamma stimulating activity is equivalent to ACE-I for the treatment of hypertension.
机译:尽管长期给予血管紧张素转化酶抑制剂(ACE-I)(如醛固酮突破),但醛固酮的产生会引起血管损伤,并且可能发生。血管紧张素II受体阻滞剂(ARB)替米沙坦可以用作过氧化物酶体增殖物激活受体(PPAR)γ的配体。已证明刺激PPARγ可以增加脂联素的产生并抑制1型血管紧张素II受体的表达。因此,我们研究了ACE-I培哚普利erbumin(培哚普利)和ARB替米沙坦对血浆醛固酮和脂联素的影响。原发性高血压患者被随机分配接受48周培哚普利(2-8 mg / d)或替米沙坦(20-80 mg / d)。我们在第0、8、24和48周测量了脂联素,醛固酮,血管紧张素II和肾素。共有53名受试者被随机分组​​。有51位受试者的数据(培哚普利组25位,替米沙坦组26位;平均年龄65.1岁)可供分析。替米沙坦(69.9 +/- 5.6至58.1 +/- 5.4 pg / mL)和培哚普利(74.1 +/- 4.7至64.7 +/- 5.3 pg / mL)组的血浆醛固酮均在第8周显着下降,但恢复到培哚普利组在第24周时的基线(67.9 +/- 4.1 pg / mL)。两组治疗后血浆糖化血红蛋白或尿白蛋白水平均无明显变化。替米沙坦在抑制醛固酮和提高脂联素水平方面比培哚普利更有效。但是,未检测到胰岛素敏感性和蛋白尿改善。这些结果与这样的想法是一致的,即使用具有PPARγ刺激活性的ARB与治疗高血压的ACE-I等效。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号