Role of the renin-angiotensin-aldosterone system in collecting duct-derived endothelin-1 regulation of blood pressure.
Role of the renin-angiotensin-aldosterone system in collecting duct-derived endothelin-1 regulation of blood pressure.
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肾素-血管紧张素-醛固酮系统在集合管源性内皮素-1 血压调节中的作用。
DOI：
10.1139/y08-028
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发表时间：
2008
影响因子：
2.1
通讯作者：
D. Kohan
中科院分区：
文献类型：
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作者：
Yuqiang Ge;Yufeng Huang;D. Kohan
肾集合管 (CD) 特异性敲除内皮素-1 (ET-1) 会导致高血压和钠排泄受损。先前的一项研究指出，在这些基因敲除 (KO) 小鼠中未能抑制肾素-血管紧张素-醛固酮轴，因此当前的研究旨在检查该系统在 CD ET-1 KO 中的作用。在正常钠摄入期间，CD ET-1 KO 小鼠和对照小鼠肾脏中的肾素含量相似；在 KO 和对照中，高钠摄入量对肾脏肾素含量的抑制程度相似。血浆肾素浓度与肾肾素含量的变化平行。缬沙坦是一种血管紧张素受体阻滞剂 (ARB)，在正常钠摄入期间消除了 CD ET-1 KO 小鼠的高血压。高钠摄入+ ARB 治疗会增加 CD ET-1 KO 患者的血压，但在对照组中则不然。高钠摄入量与 CD ET-1 KO 动物中钠排泄减少相关，但未发现水排泄或肌酐清除率发生变化。螺内酯是一种醛固酮拮抗剂，在正常钠摄入期间也可使 CD ET-1 KO 小鼠的血压正常化，而高钠摄入+螺内酯仅使 CD ET-1 KO 动物的血压升高。总之，CD ET-1 KO 患者的高血压部分是由于血管紧张素 II 和醛固酮所致。我们推测 CD 衍生的 ET-1 可能通过一种新途径调节肾脏肾素的产生。
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.
Oishi.R.：“Endothelin-1 抑制大鼠内髓集合管中 AVP 刺激的渗透水渗透性。”
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