Effects of chronic ACE inhibition on sympathetic nerve traffic and baroreflex control of circulation in heart failure

Guido Grassi, Bianca M. Cattaneo, Gino Seravalle, Antonio Lanfranchi, Massimo Pozzi, Alberto Morganti, Stefano Carugo, Giuseppe Mancia

Research output: Contribution to journalArticlepeer-review


Background: In congestive heart failure ACE inhibitors chronically reduce plasma norepinephrine. No information exists, however, on whether and to what extent this reduction reflects a true chronic inhibition of sympathetic outflow and which mechanisms may be responsible. Methods and Results: In 24 patients aged 60.3±2.0 years (mean±SEM) affected by congestive heart failure (New York Heart Association class II) and treated with diuretics and digitalis, we measured mean arterial pressure (Finapres), plasma renin activity and angiotensin II levels (radioimmunoassay), plasma norepinephrine (high-performance liquid chromatography), and muscle sympathetic nerve activity (microneurography at a peroneal nerve) at rest and during baroreceptor stimulation and deactivation caused by stepwise intravenous infusions of phenylephrine and nitroprusside, respectively. In 12 patients measurements were repeated after a 2-month addition of the ACE inhibitor benazepril (10 mg/d PO), while in the remaining 12 patients they were performed again after 2 months without any treatment modifications. Benazepril did nor alter mean arterial pressure, markedly increased plasma renin activity, reduced plasma angiotensin II, and caused a nonsignificant reduction in plasma norepinephrine. In contrast, muscle sympathetic nerve traffic was significantly reduced (-30.5±5.3%, P

Original languageEnglish
Pages (from-to)1173-1179
Number of pages7
Issue number4
Publication statusPublished - Aug 19 1997


  • Angiotensin
  • Baroreceptors
  • Heart failure
  • Nervous system
  • Reflex
  • Renin

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine

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