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

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

[Article in German]

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

[Article in German]
J Brod et al. Klin Wochenschr. .

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.

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