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肾性高血压的发病机制(作者译)

[Pathogenesis of renal hypertension (author's transl)].

作者信息

Brod J, Bahlmann J, Cachovan M, Hubrich W, Hundeshagen H

出版信息

Klin Wochenschr. 1980 Jul 15;58(14):719-26. doi: 10.1007/BF01478459.

Abstract

99 patients with a chronic renal disease (glomerulonephritis, pyelonephritis, polycystic kidneys) with a GFR reduced to 2/3 normal and without anaemia were subjected to detailed haemodynamic investigation. The earliest haemodynamic abnormality was found even before the blood pressure became elevated. This consisted in a rise of the cardiac output. Ist most likely cause was an increase in the circulating blood volume. As the arteriolar and capacitance vessels adjusted to it, the blood pressure remained unchanged and the central venous pressure slightly decreased. Blood pressure rises, when this vascular adjustment subsides. At this moment the raised blood volume will drop to normal. These changes do not correlate with the minor fluctuations of the PRA which obviously are not responsible for the subsidance of the vascular adjustment and for the rise of blood pressure.

摘要

99例慢性肾病(肾小球肾炎、肾盂肾炎、多囊肾)患者,肾小球滤过率降至正常的2/3且无贫血,接受了详细的血流动力学检查。甚至在血压升高之前就发现了最早的血流动力学异常。这表现为心输出量增加。其最可能的原因是循环血容量增加。随着小动脉和容量血管对此进行调整,血压保持不变,中心静脉压略有下降。当这种血管调节消退时,血压升高。此时升高的血容量将降至正常。这些变化与肾素活性的微小波动无关,显然肾素活性的微小波动与血管调节的消退和血压升高无关。

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