B-TYPE
NATRIURETIC PEPTIDE (BNP), BUT NOT ATRIAL NATRIURETIC PEPTIDE (ANP), IMPROVES
HAEMODYNAMICS IN ACUTE HEART FAILURE. R.L. Woods*#, H.P.
Brunner-La Rocca, D.M. Kaye and M.D. Esler. Baker Medical Research Institute,
Prahran, and #Howard Florey Institute, University of Melbourne,
3010, Australia. Experimental acute heart failure (AHF), induced by rapid cardiac
pacing, causes inadequate cardiac pump function and hemodynamic
consequences similar to that seen in humans after myocardial infarction.
Increased atrial pressures in AHF result in substantial release
of atrial natriuretic peptide (ANP), but minimal changes in B-type
natriuretic peptide (BNP). Could there be a difference in
responsiveness to ANP and BNP in the acute condition? We investigated
this possibility by infusing equimolar doses of ANP and BNP (10
pmol/kg per min) into anaesthetised dogs (n = 8) with AHF induced
by rapid right ventricular pacing (193 ± 4 bpm) to increase
pulmonary capillary wedge pressure (PCWP) to ~ 15mmHg. After
haemodynamics had stabilised (~ 45 min), randomised infusions of
ANP or BNP, or sodium nitroprusside (SNP, 0.5 mg/kg per min) for
comparison, were administered for 30min. Acute pacing reduced (P<0.05)
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 ± 2.1mmHg),
and raised (P<0.05) PCWP (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
23.4 ± 2.6 to 29.1 ± 2.3 mmHg/l.min-1).
Infusions of BNP and SNP, respectively, improved CO (+13 ±
3 % & +9 ± 5 %) by reducing pre-load (PCWP -12 ±
2 % & -12 ± 2 % and RAP -28 ± 9 % & ‑-34
± 6 %) and after-load (SVR -15 ± 4 % & -11 ±
3 %) (all p<0.01, except CO with SNP, ns). By contrast,
ANP did not significantly affect cardiac or peripheral haemodynamics.
The ineffectiveness of ANP in AHF may result from a rapid desensitisation
of the natriuretic peptide type A receptor, at high levels of ANP
in vivo. We propose that the marked haemodynamic differences
between exogenous BNP and ANP may be due to a BNP-selective receptor
that is yet to be identified.
