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肾血管减压机制:通过化学性肾髓质切除进行特征描述。

Renal vasodepressor mechanism: characterization by chemical medullectomy.

作者信息

Swales J D, Bing R F, Edmunds M E, Russell G I

机构信息

Department of Medicine, University of Leicester, United Kingdom.

出版信息

Am J Med Sci. 1988 Apr;295(4):241-5. doi: 10.1097/00000441-198804000-00004.

Abstract

The features of hypertension produced in the rat by chemical medullectomy with 2-bromoethylamine hydrobromide are described. This procedure partially prevents the fall in blood pressure that occurs when the constriction is removed from the renal artery of rats with two-kidney one-clip Goldblatt hypertension. In normal rats, chemical medullectomy causes a moderate but consistent blood pressure elevation that is dose related and associated with elevation of peripheral resistance; the venous side of the circulation is normal. The hypertension is not associated with sodium retention or with activation of the renin angiotensin system. Although vasopressin levels are elevated, the rise is only modest, and blood pressure is not reduced by a vascular AVP antagonist. It is concluded that chemical medullectomy removes the source of a humoral substance that has been shown by other workers to carry out a vasodepressor role. The chemical medullectomy model therefore offers new insights into the renomedullary vasodepressor system.

摘要

描述了用氢溴酸2-溴乙胺进行化学性髓质切除在大鼠中产生的高血压特征。该操作部分地阻止了从两肾一夹型Goldblatt高血压大鼠肾动脉解除缩窄时出现的血压下降。在正常大鼠中,化学性髓质切除会导致适度但持续的血压升高,这与剂量相关且与外周阻力升高有关;循环的静脉侧正常。高血压与钠潴留或肾素-血管紧张素系统的激活无关。尽管血管加压素水平升高,但升高幅度仅适度,且血管性抗血管加压素拮抗剂不会降低血压。得出的结论是,化学性髓质切除消除了一种体液物质的来源,其他研究人员已表明该物质具有血管减压作用。因此,化学性髓质切除模型为肾髓质血管减压系统提供了新的见解。

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