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在高压灌注下离体肾脏分泌髓质素I。

Secretion of medullipin I by isolated kidneys perfused under elevated pressure.

作者信息

Muirhead E E, Brooks B, Byers L W, Brown P, Pitcock J A

机构信息

Department of Pathology, University of Tennessee, Memphis.

出版信息

Clin Exp Pharmacol Physiol. 1991 Jun;18(6):409-17. doi: 10.1111/j.1440-1681.1991.tb01472.x.

Abstract
  1. Medullipin I (Med I) is a hormone extracted from renal papillae and its renomedullary interstitial cells (RIC). Med I is stimulated by elevation of the renal artery perfusion pressure. 2. When isolated normal rat kidneys were perfused either with oxygenated blood or with 5% albumin bubbled with O2 at elevated perfusion pressures, Med I appeared to be secreted into the renal venous effluent (RVE). Addition of Tween 20, treatment of the assay rat with SKF 525A, inhibitor of cytochrome P-450 and removal of the liver from the systemic circulation prevented vasodepression of both the RVE and extracted Med I. The lipid in the RVE gave the same dose-response as extracted Med I. 3. Lowering the renal artery perfusion pressure below normal inhibited the secretion of Med I. As the perfusion pressure was elevated Med I secretion appeared to increase. 4. Previous observations and the present study support the view that the renin-angiotensin system and the Medullipin system are double feedback systems involved in blood pressure control.
摘要
  1. 髓质素I(Med I)是一种从肾乳头及其肾髓质间质细胞(RIC)中提取的激素。肾动脉灌注压升高会刺激Med I的分泌。2. 当用含氧血液或在升高的灌注压力下用氧气鼓泡的5%白蛋白灌注离体正常大鼠肾脏时,Med I似乎会分泌到肾静脉流出液(RVE)中。添加吐温20、用细胞色素P - 450抑制剂SKF 525A处理实验大鼠以及将肝脏从体循环中移除,可防止RVE和提取的Med I的血管舒张作用。RVE中的脂质产生了与提取的Med I相同的剂量反应。3. 将肾动脉灌注压降至正常以下会抑制Med I的分泌。随着灌注压力升高,Med I的分泌似乎会增加。4. 先前的观察结果和本研究支持这样一种观点,即肾素 - 血管紧张素系统和髓质素系统是参与血压控制的双重反馈系统。

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