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低剂量慢性输注血管紧张素II所致的“缓慢升压型”高血压

'Slow pressor' hypertension from low-dose chronic angiotensin II infusion.

作者信息

Edgley A, Kett M, Anderson W

机构信息

Department of Physiology, Monash University, Victoria, Australia.

出版信息

Clin Exp Pharmacol Physiol. 2001 Dec;28(12):1035-9. doi: 10.1046/j.1440-1681.2001.03590.x.

Abstract
  1. Angiotensin (Ang) II causes growth-related effects on vascular smooth muscle cells in vitro and in vivo. 2. Chronic infusions of AngII systemically, at doses that are initially subpressor, result in slowly progressive increases in arterial pressure ('slow-pressor' hypertension). It has been suggested that the hypertension is due to induced growth in systemic resistance vessel walls by the AngII infusions. 3. We report the results of several studies investigating whether there are also induced structural changes in renal resistance vessels during chronic AngII infusions. We have developed models in Sprague-Dawley rats in which low-dose AngII infusions, either into the renal artery (thus restricting the effects to the kidney) or systemically, result in hypertension. 5. In both models, we have evidence suggesting that chronic AngII infusions have resulted in apparent structurally induced reductions in renal vasculature lumen upstream to the glomerulus. 6. The role of these renal changes in the development of the hypertension remain to be determined.
摘要
  1. 血管紧张素(Ang)II在体外和体内均可对血管平滑肌细胞产生与生长相关的作用。2. 以最初低于降压阈值的剂量全身性慢性输注AngII,会导致动脉血压缓慢进行性升高(“缓慢升压型”高血压)。有人认为,高血压是由于AngII输注导致全身阻力血管壁生长所致。3. 我们报告了几项研究的结果,这些研究旨在调查在慢性输注AngII期间肾阻力血管是否也会发生结构变化。我们在斯普拉格-道利大鼠中建立了模型,低剂量AngII输注到肾动脉(从而将作用局限于肾脏)或全身性输注,均可导致高血压。5. 在这两种模型中,我们都有证据表明,慢性输注AngII导致肾小球上游肾血管系统管腔出现明显的结构诱导性缩小。6. 这些肾脏变化在高血压发展中的作用尚待确定。

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