European Journal of Clinical Pharmacology

, Volume 33, Issue 3, pp 249–254 | Cite as

Effect of captopril on renin and blood pressure in cirrhosis

  • B. Stanek
  • F. Renner
  • A. Sedlmayer
  • K. Silberbauer


In hepatic cirrhosis neurohumoral vasoconstrictor systems are activated to compensate for circulatory disturbances. To study the renin-angiotensin-aldosterone system in more detail, angiotensin converting enzyme in 15 patients with advanced liver disease was inhibited with captopril after moderate sodium restriction.

Captopril caused an increase in plasma renin activity (p<0.005) and a decrease in plasma aldosterone (p<0.025) from an elevated baseline, and a moderate drop in systolic (p<0.025) and diastolic (p<0.05) blood pressure. Hyperreninaemia after captopril was inversely related to the prevailing plasma sodium level (r=−0.66,p<0.01), and the changes in both systolic and diastolic blood pressure were correlated with baseline plasma renin activity (r=0.49,p<0.05 for systolic andr=0.71,p<0.01 for diastolic blood pressure). No change occurred in heart rate or in stimulated plasma noradrenaline and vasopressin levels.

The data suggest that in these cirrhotic patients the reactivity of the renin-angiotensin-aldosterone system was still intact, although it occurred at a higher level. They confirm the importance of the renin-angiotensin-aldosterone system in arterial blood pressure regulation in cirrhosis.

Key words

liver cirrhosis captopril renin-angiotensin system blood pressure aldosterone 


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Copyright information

© Springer-Verlag 1987

Authors and Affiliations

  • B. Stanek
    • 1
  • F. Renner
    • 2
  • A. Sedlmayer
    • 2
  • K. Silberbauer
    • 1
    • 3
  1. 1.2nd Department of Internal MedicineUniversity of ViennaViennaAustria
  2. 2.2nd Department of Gastroenterology and Hepatology, Ludwig Boltzmann-Institute for Clinical EndocrinologyUniversity of ViennaViennaAustria
  3. 3.Krankenhaus der Barmherzigen BrüderEisenstadtAustria

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