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血管加压素与慢性肾衰竭的发病机制

Vasopressin and the pathogenesis of chronic renal failure.

作者信息

Brooks D P, Solleveld H A, Contino L C

机构信息

Department of Pharmacology, SmithKline Beecham Pharmaceuticals, King of Prussia, PA 19406.

出版信息

Br J Pharmacol. 1990 May;100(1):79-82. doi: 10.1111/j.1476-5381.1990.tb12055.x.

DOI:10.1111/j.1476-5381.1990.tb12055.x
PMID:2372662
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1917451/
Abstract
  1. Partial (5/6) renal ablation was performed in Long Evans rats treated with vehicle or a vasopressin V1-receptor antagonist, in control Long Evans rats, and in homozygous Brattleboro rats which lack endogenous vasopressin. 2. In control and vasopressin-blocked Long Evans rats, 3 weeks following partial renal ablation, systolic blood pressure was 215 +/- 5 and 199 +/- 9 mmHg and, urinary protein excretion was 54 +/- 4 and 50 +/- 3 mg day-1, respectively. 3. The pressor response to exogenous vasopressin was significantly (P less than 0.05) reduced in rats treated with the V1-receptor antagonist (ED50 mmHg 5.0 +/- 1.6 vs. 0.09 +/- 0.01 micrograms kg-1). 4. In control Long Evans and in Brattleboro rats, 3 weeks following renal ablation, systolic blood pressure was 204 +/- 10 and 191 +/- 7 mmHg, and urinary protein excretion was 97 +/- 27 and 71 +/- 5 mg day-1, respectively. 5. Histological examination of the remaining kidney tissue demonstrated significant glomerular hyalinization following renal ablation but no differences between any of the groups. 6. The data indicate that neither vasopressin nor the urinary concentrating mechanism is likely to be involved in the hypertension and proteinuria associated with partial renal ablation.
摘要
  1. 对用赋形剂或血管加压素V1受体拮抗剂处理的Long Evans大鼠、对照Long Evans大鼠以及缺乏内源性血管加压素的纯合Brattleboro大鼠进行部分(5/6)肾切除。2. 在对照和血管加压素阻断的Long Evans大鼠中,部分肾切除3周后,收缩压分别为215±5和199±9 mmHg,尿蛋白排泄分别为54±4和50±3 mg/天。3. 用V1受体拮抗剂处理的大鼠对外源性血管加压素的升压反应显著降低(P<0.05)(ED50 mmHg 5.0±1.6 vs. 0.09±0.01微克/千克)。4. 在对照Long Evans大鼠和Brattleboro大鼠中,肾切除3周后,收缩压分别为204±10和191±7 mmHg,尿蛋白排泄分别为97±27和71±5 mg/天。5. 对剩余肾组织的组织学检查显示肾切除后有明显的肾小球玻璃样变,但各实验组间无差异。6. 数据表明,血管加压素和尿液浓缩机制均不太可能参与部分肾切除相关的高血压和蛋白尿。

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引用本文的文献

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Vasopressin in chronic kidney disease: an elephant in the room?慢性肾脏病中的血管加压素:被忽视的重要问题?
Kidney Int. 2009 Nov;76(9):925-8. doi: 10.1038/ki.2009.325.

本文引用的文献

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Vasopressin in the rat with partial nephrectomy-salt hypertension.去甲肾上腺素在部分肾切除-盐性高血压大鼠中的作用
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[1-beta-Mercapto-beta,beta-cyclopentamethylenepropionic acid),2-(O-methyl)tyrosine ]argine-vasopressin and [1-beta-mercapto-beta,beta-cyclopentamethylenepropionic acid)]argine-vasopressine, two highly potent antagonists of the vasopressor response to arginine-vasopressin.[1-β-巯基-β,β-环戊亚甲基丙酸],2-(O-甲基)酪氨酸]精氨酸加压素和[1-β-巯基-β,β-环戊亚甲基丙酸]精氨酸加压素,两种对精氨酸加压素的升压反应具有高度强效的拮抗剂。
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AVP-induced Ca fluxes and contraction of rat glomerular mesangial cells.血管加压素诱导的大鼠肾小球系膜细胞钙通量和收缩
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Role of vasopressin in cardiovascular regulation.血管加压素在心血管调节中的作用。
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Control of glomerular hypertension limits glomerular injury in rats with reduced renal mass.控制肾小球高血压可限制肾质量减少大鼠的肾小球损伤。
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Arginine vasopressin promotes growth of rat glomerular mesangial cells in culture.精氨酸加压素可促进培养的大鼠肾小球系膜细胞生长。
Am J Physiol. 1988 Nov;255(5 Pt 2):F898-906. doi: 10.1152/ajprenal.1988.255.5.F898.
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Vasopressin receptors from cultured mesangial cells resemble V1a type.来自培养的系膜细胞的血管加压素受体类似于V1a型。
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Renal microvascular effects of vasopressin and vasopressin antagonists.
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Glomerular hemodynamic changes vs. hypertrophy in experimental glomerular sclerosis.实验性肾小球硬化中肾小球血流动力学变化与肥大的对比
Kidney Int. 1989 Feb;35(2):654-60. doi: 10.1038/ki.1989.35.