[Pathogenesis of renal hypertension (author's transl)].
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.
D001794:Blood Pressure; D001810:Blood Volume; D002302:Cardiac Output; D005919:Glomerular Filtration Rate; D005921:Glomerulonephritis / Q000150:complications; D006439:Hemodynamics; D006801:Humans; D006977:Hypertension, Renal / Q000209:etiology / Q000503:physiopathology*; D007690:Polycystic Kidney Diseases / Q000150:complications; D011704:Pyelonephritis / Q000150:complications
Pathogenese des renalen Hochdrucks.