Atrial natriuretic peptide augments the variability of sympathetic nerve activity in human heart failure

Citation
T. Kubo et al., Atrial natriuretic peptide augments the variability of sympathetic nerve activity in human heart failure, J HYPERTENS, 19(3), 2001, pp. 619-626
Citations number
32
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Journal title
JOURNAL OF HYPERTENSION
ISSN journal
02636352 → ACNP
Volume
19
Issue
3
Year of publication
2001
Part
2
Pages
619 - 626
Database
ISI
SICI code
0263-6352(200103)19:3<619:ANPATV>2.0.ZU;2-#
Abstract
Objectives Activation of the sympathetic nervous system, decreased heart ra te variability (HRV), and loss of modulation of muscle sympathetic nerve ac tivity (MSNA) within the low frequency (LF, 0.05-0.15 Hz) range are three a dverse features of advanced congestive heart failure (CHF). In healthy men, atrial natriuretic peptide (ANP) infusion attenuates reflex increases in M SNA and reduces LF components of HRV spectral power. Sympathoinhibitory act ions have also been documented in CHF, but effects on the variability of MS NA and HRV have not been described. Design and methods Heart rate and MSNA were recorded in 10 men (aged 39 +/- 3 years, mean +/- SE) with dilated cardiomyopathy (mean EF 20 +/- 4%) trea ted with angiotensin converting enzyme (ACE) inhibitors. Subjects received i.v. ANP (50 mug bolus then 50 ng/kg/min) and nitroglycerin (NTG, 8 mg/min) as a hemodynamic control. Signals at baseline, and 13-20 min into each inf usion were submitted to spectral analysis. Results ANP had no effect on HRV, but increased MSNA LF (from 7.9 +/- 1.5 t o 12.1 +/- 2.6 U-2; P < 0.02) and total spectral power (from 47.9 <plus/min us> 5.4 to 61.9 +/- 6.8 U-2; P < 0.05). NTG had no effect on the variabilit y of MSNA or HRV. Conclusions In CHF patients receiving ACE inhibitors, ANP (i) does not supp ress HRV and (ii) enhances the modulation of MSNA, particularly within the LF range. This latter action is not observed with NTG, These findings sugge st beneficial actions of exogenous ANP on neurogenic circulatory control.