Interrelationships between blood pressure, renin, renin substrate and blood volume in terminal renal failure.

نویسندگان

  • M A Schalekamp
  • M P Schalekamp-Kuyken
  • M de Moor-Fruytier
  • T Meininger
  • D J Vaandrager-Kranenburg
  • W H Birkenhäger
چکیده

1. The effect of haemodialysis on blood pressure was assessed in forty-six patients with end-stage kidney disease, in relation to measurements of plasma renin concentration (PRC), plasma renin substrate (PRS) and blood volume. Parallel measurements of PRC and blood volume were carried out before and during the period of regular dialysis treatment. PRS was measured during this period only. 2. Both before and during regular dialysis PRC was higher in relation to blood volume in patients whose hypertension persisted after fluid withdrawal than in cases who became normotensive. PRS levels were similar in both groups. 3. The decrease of blood volume by regular dialysis led to a rise in plasma renin both in patients with controllable hypertension and in those with persistent hypertension. After at least 5 months of regular dialysis, the acute removal of 1.5 litres of body fluid caused a similar percentage rise in PRC in six patients with persistent hypertension and twelve patients with controllable hypertension. In three other patients with controllable hypertension and very low PRC, PRC was unresponsive both to the acute and the chronic volume depletion. 4. The pressor response to exogenous angiotensin in anephric patients, in whom no renin could be detected in the plasma, was decreased after ultrafiltration. This was caused by an increase in the threshold dose and not by a decrease in the slope of the dose-response relationship. This effect of ultrafiltration was due to fluid loss itself rather than to a rise in endogenous angiotensin. 5. The results indicate that the presence of hypertension in the face of fluid loss reflects a disturbance in renin release which is rather associated with the pathologic state of the kidney than with an excessive stimulus to the kidney. The decrease in sensitivity to angiotensin caused by fluid loss is presumably overridden by the effect of a high renin level.

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عنوان ژورنال:
  • Clinical science and molecular medicine

دوره 45 4  شماره 

صفحات  -

تاریخ انتشار 1973