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肾脏在高血压发病中的作用:布拉格高血压大鼠的移植研究

The role of the kidney in the development of hypertension: a transplantation study in the Prague hypertensive rat.

作者信息

Heller J, Schubert G, Havlíckova J, Thurau K

机构信息

Department of Experimental Medicine, Institute for Clinical Experimental Medicine, Prague, Czech Republic.

出版信息

Pflugers Arch. 1993 Nov;425(3-4):208-12. doi: 10.1007/BF00374168.

DOI:10.1007/BF00374168
PMID:8309780
Abstract

It has been shown that genetic hypertension in rats usually "travels with the kidney". To elucidate the mechanism of this phenomenon further, experiments were carried out in the Prague hypertensive (PH) rat, a model of genetic hypertension derived from the Wistar strain, in which a normotensive parallel, the Prague normotensive (PN) rat, was also bred from the same parent pair. Thus, it is possible to transfer organs between both parallels without substantial signs of rejection and without the use of immunosuppressive drugs. Unilateral nephrectomy and transplantation of one kidney between PH and PN rats, did not affect the arterial blood pressure (BP). Transplantation of one kidney from PN rats to bilaterally nephrectomised PH rats normalised the high BP. If a PH rat was left with one original kidney in situ after the transplantation of a "normotensive" kidney, the high BP persisted until the original "hypertensive" kidney was removed. This removal resulted in sustained normalisation of BP. When the development of high BP in the PH rats was prevented for 2 months after weaning by antihypertensive drugs, transplantation of kidneys from these rats to bilaterally nephrectomised PN rats always induced a sustained hypertension in the recipient. These results argue against a role of high-BP-induced damage to the kidney and against an intrinsic increase in the salt-reabsorptive capacity of the tubular epithelium in PH rats. The data support the view that the kidney from PH rats produces a "hypertensinogenic" substance, the secretion of which is genetically determined and is not influenced by the magnitude of the BP.

摘要

研究表明,大鼠的遗传性高血压通常“与肾脏相关”。为了进一步阐明这一现象的机制,我们以布拉格高血压(PH)大鼠为实验对象进行了实验,该大鼠是源自Wistar品系的遗传性高血压模型,同时还培育了与之血压正常的对照品系——布拉格正常血压(PN)大鼠,它们来自同一亲本对。因此,有可能在这两个品系之间进行器官移植,而不会出现明显的排斥迹象,也无需使用免疫抑制药物。对PH大鼠和PN大鼠进行单侧肾切除术,并在两者之间移植一个肾脏,并未影响动脉血压(BP)。将PN大鼠的一个肾脏移植到双侧肾切除的PH大鼠体内,可使高血压恢复正常。如果在移植“正常血压”肾脏后,让PH大鼠保留一个原位的原肾,高血压会持续存在,直到切除原有的“高血压”肾脏,血压才会持续恢复正常。当通过抗高血压药物在断奶后2个月内防止PH大鼠出现高血压时,将这些大鼠的肾脏移植到双侧肾切除的PN大鼠体内,总会使受体大鼠出现持续性高血压。这些结果表明,高血压引起的肾脏损伤以及PH大鼠肾小管上皮细胞盐重吸收能力的内在增加,均与高血压的发生无关。这些数据支持以下观点:PH大鼠的肾脏会产生一种“致高血压”物质,其分泌由基因决定,不受血压水平的影响。

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Na/K-ATPase Signaling and Salt Sensitivity: The Role of Oxidative Stress.钠钾ATP酶信号传导与盐敏感性:氧化应激的作用
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Renal Dysfunction, Rather Than Nonrenal Vascular Dysfunction, Mediates Salt-Induced Hypertension.介导盐诱导高血压的是肾功能不全,而非非肾血管功能不全。

本文引用的文献

1
The Prague Hypertensive Rat: a new model of genetic hypertension.布拉格高血压大鼠:一种遗传性高血压的新模型。
Clin Exp Hypertens. 1993 Sep;15(5):807-18. doi: 10.3109/10641969309041643.
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Pflugers Arch. 1996 Apr;431(6):971-6. doi: 10.1007/s004240050093.
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Hypertension in renal allograft recipients may be conveyed by cadaveric kidneys from donors with subarachnoid haemorrhage.肾移植受者的高血压可能由患有蛛网膜下腔出血的供体的尸体肾脏传播。
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Effects of interstrain renal transplantation on NaCl-induced hypertension in Dahl rats.品系间肾移植对 Dahl 大鼠盐诱导高血压的影响。
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Role of the kidney in the pathogenesis of primary hypertension.肾脏在原发性高血压发病机制中的作用。
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Role of the kidney in primary hypertension: a renal transplantation study in rats.肾脏在原发性高血压中的作用:大鼠肾移植研究
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