Divergent effects of ANP and BNP in acute heart failure: evidence for a putative BNP-selective receptor?
OBJECTIVE
Since the pathophysiology of natriuretic peptides in chronic heart failure (HF) is not uniform, we hypothesized that atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) may also have differential effects in acute HF. Our aim was to compare the haemodynamic actions of ANP with BNP, using a classical vasodilator as the control, in greyhound dogs with acute pacing-induced HF.


METHODS
The right ventricles of eight anaesthetized dogs were paced (193 +/- 4 bpm) until pulmonary capillary pressure (PCP) increased to approximately 15 mmHg. In each animal, according to a randomized within-animal design, haemodynamic responses to equimolar (10 pmol/kg per min) infusions of ANP and BNP were compared with those to sodium nitroprusside (SNP).


RESULTS
Acute pacing alone increased PCP from 6.6 +/- 0.7 to 15.7 +/- 0.3 mmHg, right atrial pressure (RAP) from 1.9 +/- 0.5 to 4.0 +/- 0.6 mmHg, and systemic vascular resistance (SVR) from 1706 +/- 110 to 2179 +/- 106 dyne s/cm5, and reduced cardiac output (CO) from 4.1 +/- 0.4 to 2.5 +/- 0.2 l/min and arterial pressure from 86.1 +/- 2.4 to 74.5 +/- 2.1 mmHg (all P < 0.01). BNP and SNP improved haemodynamics similarly (CO +13 +/- 3% and +9 +/- 5%; PCP -12 +/- 2% and -12 +/- 2%; RAP -28 +/- 9% and -34 +/- 6%, SVR -15 +/- 3% and -11 +/- 3%, all P < 0.01, except CO with SNP, not significant), but effects of BNP on preload outlasted those of SNP. By contrast, ANP did not improve the haemodynamics. Haematocrit was significantly higher during BNP infusion than with ANP (P < 0.05) or with SNP (P < 0.001).


CONCLUSIONS
The haemodynamic responses to exogenous BNP and ANP in acute heart failure were strikingly different. Whereas ANP actions were blunted, BNP response was preserved. Hypothetically, the presence of a putative BNP receptor may explain this finding.
Brunner-La Rocca
Hans Peter
HP
Baker Medical Research Institute, Melbourne, Australia. hanspeter.brunner@dim.usz.ch
Woods
Robyn L
RL
Kaye
David M
DM
Hastings
Jacqueline
J
Thomas
Colleen J
CJ
Lambert
Elisabeth
E
Esler
Murray D
MD
D000208:Acute Disease; D000818:Animals; D016280:Atrial Function, Right / Q000187:drug effects; D009320:Atrial Natriuretic Factor / Q000494:pharmacology*; D001794:Blood Pressure / Q000187:drug effects; D002302:Cardiac Output / Q000187:drug effects; D002303:Cardiac Output, Low / Q000503:physiopathology*; D002304:Cardiac Pacing, Artificial; D004285:Dogs; D005260:Female; D006400:Hematocrit; D006439:Hemodynamics / Q000187:drug effects; D008297:Male; D020097:Natriuretic Peptide, Brain / Q000494:pharmacology*; D009599:Nitroprusside / Q000494:pharmacology; D011669:Pulmonary Wedge Pressure / Q000187:drug effects; D017461:Receptors, Atrial Natriuretic Factor / Q000378:metabolism; D014655:Vascular Resistance / Q000187:drug effects; D014665:Vasodilator Agents / Q000494:pharmacology
D014665:Vasodilator Agents; C058930:brain natriuretic peptide receptor; D020097:Natriuretic Peptide, Brain; D009599:Nitroprusside; D009320:Atrial Natriuretic Factor; D017461:Receptors, Atrial Natriuretic Factor