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戈德布拉特高血压大鼠的盐敏感性——细胞外液容量和肾素-血管紧张素系统的作用

Salt sensitivity in Goldblatt hypertensive rats--role of extracellular fluid volume and renin-angiotensin system.

作者信息

Sato Y, Ando K, Ogata E, Fujita T

机构信息

Fourth Department of Internal Medicine, School of Medicine University of Tokyo, Japan.

出版信息

Jpn Circ J. 1991 Feb;55(2):165-73. doi: 10.1253/jcj.55.165.

Abstract

Effects of a high-salt diet on blood pressure, extracellular fluid volume, and the renin-angiotensin system in rats with the two types of Goldblatt hypertension were examined. Both in one-kidney, one clip (1K1C) rats and in one-kidney, sham-clipped (1K) rats, systolic blood pressures of rats which received a high-salt diet for 4 weeks were higher than those of rats of respective groups on a normal-salt diet, suggesting an increased sensitivity of blood pressure to changes in salt intake. Whereas sodium space was increased in 1K rats on the high-salt 1K1C rats receiving the high-salt did not have significantly increased sodium space. These results suggest that acceleration of 1K1C hypertension with salt load could not be explained only by changes in extracellular fluid volume. In contrast, both in two-kidney, one clip (2K1C) rats and in two-kidney, sham-clipped (2K) rats, the high-salt diet produced no change in blood pressure despite the increase in sodium space, suggesting a decreased salt sensitivity. Although on the normal-salt diet the blood pressure of 2K1C rats tended to correlate with plasma renin activity, on the high-salt diet plasma renin activity was markedly decreased, and then blood pressure highly correlated with sodium space. Accordingly, the lesser salt sensitivity in 2K1C rats is probably attributable to the counterbalance of the suppressed renin-angiotensin system against volume expansion. Evidence presented suggests, therefore, that 1K1C rats have greater salt sensitivity of blood pressure than 2K1C rats.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

研究了高盐饮食对两种类型戈德布拉特高血压大鼠血压、细胞外液量和肾素 - 血管紧张素系统的影响。在一侧肾、单夹闭(1K1C)大鼠和一侧肾、假夹闭(1K)大鼠中,接受高盐饮食4周的大鼠收缩压均高于各自组中正常盐饮食的大鼠,这表明血压对盐摄入量变化的敏感性增加。高盐饮食的1K大鼠钠空间增加,而接受高盐饮食的1K1C大鼠钠空间没有显著增加。这些结果表明,盐负荷加速1K1C高血压不能仅用细胞外液量的变化来解释。相反,在两侧肾、单夹闭(2K1C)大鼠和两侧肾、假夹闭(2K)大鼠中,尽管钠空间增加,但高盐饮食并未使血压发生变化,这表明盐敏感性降低。虽然在正常盐饮食时2K1C大鼠的血压倾向于与血浆肾素活性相关,但在高盐饮食时血浆肾素活性明显降低,然后血压与钠空间高度相关。因此,2K1C大鼠盐敏感性较低可能归因于肾素 - 血管紧张素系统对容量扩张的抵消作用。因此,现有证据表明,1K1C大鼠的血压盐敏感性高于2K1C大鼠。(摘要截短至250字)

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