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联体大鼠肾缺如性高血压发生中的遗传影响。有证据表明,易患高血压大鼠的肾组织中产生一种体液性高血压生成因子。

Genetic influence on the development of renoprival hypertension in parabiotic rats. Evidence that a humoral hypertensinogenic factor is produced in kidney tissue of hypertension-prone rats.

作者信息

Knudsen K D, Iwai J, Heine M, Leitl G, Dahl L K

出版信息

J Exp Med. 1969 Dec 1;130(6):1353-65. doi: 10.1084/jem.130.6.1353.

Abstract

Rats from two strains with opposite constitutional predisposition to hypertension were joined in parabiosis and one partner was nephrectomized. The influence of genetic factors and of diet on the blood pressures of the two classes of parabionts, operated and intact, indicated that renoprival hypertension occurred with equal frequency in rats from both strains; that the development of renoprival hypertension depended on the influence from an intact S partner, or on a high salt intake, or on both. A nephrectomized S rat developing renoprival hypertension did not induce high blood pressure in its intact R partner. In this respect renoprival hypertension differs from salt and renal hypertension. The findings are interpreted to mean that the hypertensinogenic agent specific for S rats is produced by S kidneys.

摘要

将具有相反体质性高血压易感性的两个品系的大鼠进行联体,并对其中一个联体伙伴进行肾切除。遗传因素和饮食对两类联体大鼠(手术组和完整组)血压的影响表明,双侧肾切除诱发的高血压在两个品系的大鼠中发生频率相同;双侧肾切除诱发的高血压的发展取决于来自完整的S伙伴的影响,或高盐摄入,或两者兼而有之。发生双侧肾切除诱发高血压的肾切除S大鼠不会在其完整的R伙伴中诱发高血压。在这方面,双侧肾切除诱发的高血压不同于盐性和肾性高血压。这些发现被解释为意味着S大鼠特有的高血压生成因子是由S肾脏产生的。

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Lost mass and excretion as stimuli to parabiotic compensatory renal hypertrophy.
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