首页> 外文期刊>American Journal of Physiology >Long-term AT1 receptor blockade improves metabolic function and provides renoprotection in Fischer-344 rats.
【24h】

Long-term AT1 receptor blockade improves metabolic function and provides renoprotection in Fischer-344 rats.

机译:长期的AT1受体阻断可改善Fischer-344大鼠的代谢功能并提供肾保护作用。

获取原文
获取原文并翻译 | 示例
           

摘要

Fischer-344 (F344) rats exhibit proteinuria and insulin resistance in the absence of hypertension as they age. We determined the effects of long-term (1 yr) treatment with the angiotensin (ANG) II type 1 (AT(1)) receptor blocker L-158,809 on plasma and urinary ANG peptide levels, systolic blood pressure (SBP), and indexes of glucose metabolism in 15-mo-old male F344 rats. Young rats at 3 mo of age (n = 8) were compared with two separate groups of older rats: one control group (n = 7) and one group treated with L-158,809 (n = 6) orally (20 mg/l) for 1 yr. SBP was not different between control and treated rats but was higher in young rats. Serum leptin, insulin, and glucose levels were comparable between treated and young rats, whereas controls had higher glucose and leptin with a similar trend for insulin. Plasma ANG I and ANG II were higher in treated than untreated young or older rats, as evidence of effective AT(1) receptor blockade. Urinary ANG II and ANG-(1-7) were higher in controls compared with young animals, and treated rats failed to show age-related increases. Protein excretion was markedly lower in treated and young rats compared with control rats (young: 8 +/- 2 mg/day vs. control: 129 +/- 51 mg/day vs. treated: 9 +/- 3 mg/day, P < 0.05). Long-term AT(1) receptor blockade improves metabolic parameters and provides renoprotection. Differential regulation of systemic and intrarenal (urinary) ANG systems occurs during blockade, and suppression of the intrarenal system may contribute to reduced proteinuria. Thus, insulin resistance, renal injury, and activation of the intrarenal ANG system during early aging in normotensive animals can be averted by renin-ANG system blockade.
机译:Fischer-344(F344)大鼠随着年龄增长而在没有高血压的情况下表现出蛋白尿和胰岛素抵抗。我们确定了使用血管紧张素(ANG)II型1(AT(1))受体阻滞剂L-158,809长期(1年)治疗对血浆和尿ANG肽水平,收缩压(SBP)和指标的影响15个月大的雄性F344大鼠体内葡萄糖代谢的变化将3个月大的年轻大鼠(n = 8)与两组单独的老年大鼠进行比较:一个对照组(n = 7)和一组口服L-158,809(n = 6)(20 mg / l)一年。对照和治疗大鼠之间的SBP没有差异,但幼鼠较高。在治疗和年轻大鼠中,血清瘦素,胰岛素和葡萄糖水平相当,而对照组的葡萄糖和瘦素水平更高,胰岛素的趋势相似。作为有效AT(1)受体阻滞的证据,治疗的血浆ANG I和ANG II高于未治疗的年轻或老年大鼠。与年幼动物相比,对照组的尿ANG II和ANG-(1-7)更高,并且治疗的大鼠未显示出与年龄相关的增加。与对照组相比,治疗组和年轻大鼠的蛋白质排泄量显着降低(年轻组:8 +/- 2 mg /天,对照组:129 +/- 51 mg /天,与治疗组:9 +/- 3 mg /天, P <0.05)。长期的AT(1)受体阻断可改善代谢参数并提供肾保护作用。阻断过程中会发生全身性和肾内(尿)ANG系统的差异调节,抑制肾内系统可能会导致蛋白尿减少。因此,可以通过肾素-ANG系统的阻断来避免血压正常动物在早期衰老过程中的胰岛素抵抗,肾损伤和肾内ANG系统的激活。

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