The correction of autonomic dysfunction in cirrhosis by captopril

J Hepatol. 1997 Feb;26(2):331-5. doi: 10.1016/s0168-8278(97)80049-9.


Background/aims: Vagal dysfunction is reported in about 70% of patients with cirrhosis, irrespective of aetiology, as detected by cardiovascular reflex tests. We have previously shown that RR-variability on 24-h ECG is a more sensitive marker of vagal dysfunction in cirrhosis. Angiotensin II inhibits vagal function in animals, and it is elevated in cirrhosis and may be the cause of the vagal dysfunction. Our aim was to observe the effect of captopril on vagal dysfunction in cirrhosis.

Methods: Eight patients with cirrhosis (biopsy proven, male two, female six, mean age 54.25) had 24-h ECG RR-variability performed. They then received captopril 25 mg t.d.s. for 48 h. The 24-h ECG was repeated on therapy.

Results: Mean blood pressure remained unchanged: baseline 89.8 +/- 4.8 mmHg (mean +/- sem) versus 91.8 +/- 5.9 mmHg, p = not significant. Median baseline RR-variability was 791 (range 18-5344) counts/24 h and increased in all but one patient, with captopril, to 1548 (56-4824) p = 0.008. Three increased into the normal range.

Conclusion: The vagal dysfunction of cirrhosis is caused by neuromodulation by angiotensin II and is not due to a neuropathy.

MeSH terms

  • Adult
  • Angiotensin II / blood
  • Angiotensin-Converting Enzyme Inhibitors / pharmacology*
  • Blood Pressure / drug effects
  • Captopril / pharmacology*
  • Electrocardiography / drug effects
  • Female
  • Humans
  • Liver Cirrhosis / physiopathology*
  • Male
  • Middle Aged
  • Reflex / drug effects
  • Vagus Nerve / drug effects
  • Vagus Nerve / physiopathology*


  • Angiotensin-Converting Enzyme Inhibitors
  • Angiotensin II
  • Captopril