Effects of intravenous brain natriuretic peptide on regional sympathetic activity in patients with chronic heart failure as compared with healthy control subjects

Citation
Hp. Brunner-la Rocca et al., Effects of intravenous brain natriuretic peptide on regional sympathetic activity in patients with chronic heart failure as compared with healthy control subjects, J AM COL C, 37(5), 2001, pp. 1221-1227
Citations number
43
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Journal title
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
ISSN journal
07351097 → ACNP
Volume
37
Issue
5
Year of publication
2001
Pages
1221 - 1227
Database
ISI
SICI code
0735-1097(200104)37:5<1221:EOIBNP>2.0.ZU;2-A
Abstract
OBJECTIVES We sought to assess the effects of brain natriuretic peptide (BN P) on systemic and regional sympathetic nervous activity (SNA) in both pati ents with congestive heart failure (CHF) and healthy control subjects. BACKGROUND Although the response of SNA to atrial natriuretic peptide (ANP) has been well documented, the response of SNA to BNP is largely unknown. METHODS We assessed cardiac and whole-body SNA using the norepinephrine (NE ) tracer dilution method before and after infusion of two doses of BNP (3 a nd 15 ng/kg body weight per min) in 11 patients with stable CHF (ejection f raction 24 +/- 2%) and 12 age-matched healthy control subjects. In addition , renal SNA and hemodynamic variables were assessed at baseline and after t he higher BNP dose. RESULTS Low dose BNP did not change blood pressure or whole-body NE spillov er, but reduced cardiac NE spillover in both groups by 32 +/- 13 pmol/min ( p < 0.05). In both groups, high dose BNP reduced pulmonary capillary pressu re by 5 +/- 1 mm Hg (p < 0.001) and mean arterial pressure by 6 +/- 3 mm Hg (p < 0.05), without a concomitant increase in whole-body NE spillover; how ever, cardiac NE spillover returned to baseline levels. Renal NE spillover remained virtually unchanged in healthy control subjects (501 +/- 120 to 56 4 +/- 115 pmol/min), but was reduced in patients with CHF (976 +/- 133 to 6 56 +/- 127 pmol/min, p < 0.01). CONCLUSIONS Our results demonstrate a sympathoinhibitory effect of BNP. Car diac sympathetic inhibition was observed at BNP concentrations within the p hysiologic range, whereas high dose BNP, when arterial and filling pressure s fell and reflex sympathetic stimulation was expected, systemic and cardia c SNA equated to baseline values. There was inhibition of renal SNA in pati ents with CHF, but not in healthy control subjects. Whether this effect is specific to BNP or related to reduced filling pressure remains to be determ ined. CT Am Coil Cardiol 2001;37: 1221-7) (C) 2001 by the American College of Cardiology.