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镉诱导高血压大鼠的钠潴留

Sodium retention in rats with cadmium-induced hypertension.

作者信息

Perry H M, Erlanger M W

出版信息

Sci Total Environ. 1981 Dec;22(1):31-8. doi: 10.1016/0048-9697(81)90079-6.

Abstract

Chronic feeding of non-toxic doses of cadmium induces an average increase of 15 to 20 mm Hg in indirectly measured systolic pressure of lightly anaesthetized rats. The mechanism of this increase is not known, but cadmium has several potentially pressor effects, including increased sodium retention. This report describes both sodium balance and blood pressure in a pair of experiments where cadmium was fed and in a pair where it was injected. All four cadmium challenges induced sodium retention and also induced hypertension. Thus, rats with either low or moderate chronic exposure to fed cadmium (well below the exposures required to induce toxicity) retained more intraperitoneally injected radiosodium than controls and at the same time developed higher systolic pressures than controls. Immediately following intraperitoneally injected cadmium, rats lost a radiosodium more rapidly than controls; in both situations the blood pressure was higher than the controls. These data indicate that some of the pressor effect associated with cadmium exposure could result from its concomitant antinatriuretic effect.

摘要

长期给轻度麻醉的大鼠喂食无毒剂量的镉,间接测量的收缩压平均升高15至20毫米汞柱。这种升高的机制尚不清楚,但镉有几种潜在的升压作用,包括钠潴留增加。本报告描述了两组实验中的钠平衡和血压情况,一组喂食镉,另一组注射镉。所有四次镉刺激均导致钠潴留并引发高血压。因此,长期低剂量或中等剂量喂食镉的大鼠(远低于诱导毒性所需的暴露量)比对照组保留了更多经腹腔注射的放射性钠,同时收缩压也高于对照组。腹腔注射镉后,大鼠比对照组更快地失去放射性钠;在这两种情况下,血压均高于对照组。这些数据表明,与镉暴露相关的一些升压作用可能是由其伴随的抗利尿钠作用导致的。

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