...
首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >Role of the renin-angiotensin-aldosterone system in collecting duct-derived endothelin-1 regulation of blood pressure.
【24h】

Role of the renin-angiotensin-aldosterone system in collecting duct-derived endothelin-1 regulation of blood pressure.

机译:肾素-血管紧张素-醛固酮系统在收集导管衍生的内皮素-1调节血压中的作用。

获取原文
获取原文并翻译 | 示例
           

摘要

Renal collecting duct (CD)-specific knockout of endothelin-1 (ET-1) causes hypertension and impaired Na excretion. A previous study noted failure to suppress the renin-angiotensin-aldosterone axis in these knockout (KO) mice, hence the current investigation was undertaken to examine the role of this system in CD ET-1 KO. Renal renin content was similar in kidneys from CD ET-1 KO and control mice during normal Na intake; high-Na intake suppressed renal renin content to a similar degree in KO and control. Plasma renin concentrations paralleled changes in renal renin content. Valsartan, an angiotensin receptor blocker (ARB), abolished the hypertension in CD ET-1 KO mice during normal Na intake. High-Na intake + ARB treatment increased blood pressure in CD ET-1 KO, but not in controls. High-Na intake was associated with reduced Na excretion in CD ET-1 KO animals, but no changes in water excretion or creatinine clearance were noted. Spironolactone, an aldosterone antagonist, also normalized blood pressure in CD ET-1 KO mice during normal Na intake, whereas high-Na intake + spironolactone raised blood pressure only in CD ET-1 KO animals. In summary, hypertension in CD ET-1 KO is partly due to angiotensin II and aldosterone. We speculate that CD-derived ET-1 may regulate, via a novel pathway, renal renin production.
机译:肾脏收集管(CD)特异性内皮素1(ET-1)的敲除会导致高血压和钠排泄受损。先前的一项研究指出未能抑制这些敲除(KO)小鼠的肾素-血管紧张素-醛固酮轴,因此,目前的研究是为了检查该系统在CD ET-1 KO中的作用。在正常摄入钠的过程中,CD ET-1 KO和对照组小鼠肾脏中的肾素含量相似。高钠摄入量在KO和对照组中将肾肾素含量抑制到相似的程度。血浆肾素浓度与肾素含量变化平行。缬沙坦,一种血管紧张素受体阻滞剂(ARB),在正常的Na摄入期间消除了CD ET-1 KO小鼠的高血压。高钠摄入+ ARB治疗可增加CD ET-1 KO的血压,但不增加对照组的血压。高Na摄入与CD ET-1 KO动物中Na排泄减少有关,但未观察到水排泄或肌酐清除率的变化。螺内酯,一种醛固酮拮抗剂,也可以在正常的Na摄入期间使CD ET-1 KO小鼠的血压正常化,而高Na摄入+螺内酯仅在CD ET-1 KO动物中使血压升高。总之,CD ET-1 KO中的高血压部分归因于血管紧张素II和醛固酮。我们推测CD衍生的ET-1可能通过新途径调节肾素的产生。

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