Circulation, Vol 89, 2232-2240, Copyright © 1994 by American Heart Association
A Wada, T Tsutamoto, Y Matsuda and M Kinoshita
BACKGROUND: To elucidate the extent of the compensatory role of endogenous
atrial natriuretic peptide (ANP) in severe congestive heart failure (CHF),
we examined the changes in hemodynamics and neuroendocrine and renal
functions after incremental administration of an ANP antagonist, HS-142-1
(HS), in dogs with CHF. METHODS AND RESULTS: We assessed the effects of HS
on the suppression of plasma and urinary cGMP levels as a marker of
endogenous ANP activity in dogs without CHF. Bolus injections of 0.3 and
1.0 mg/kg HS reduced plasma cGMP levels to 77% and 60% and urinary cGMP
excretion to 78% and 61% of the relevant control levels, respectively. Then
the study was performed in dogs with CHF induced by chronic rapid
ventricular pacing, and the plasma ANP level was sixfold higher than that
in the controls. Hemodynamic, hormonal, and renal variables were determined
both before and after subsequent incremental administration (0.3, 1.0, and
3.0 mg/kg every 30 minutes) of HS. HS lowered the plasma and urinary cGMP
levels dose dependently to 32% and 37% of the control levels, respectively.
Mean arterial, pulmonary capillary wedge, and right atrial pressures and
cardiac output did not change significantly. However, plasma renin
activity, aldosterone level, and norepinephrine level increased rapidly to
226%, 179%, and 252% of the control values, respectively. Urine flow rate
and urinary sodium excretion were significantly inhibited, with no
concomitant change in glomerular filtration rate or renal plasma flow.
CONCLUSIONS: These findings suggest that endogenous ANP contributes to the
suppression of the activation of the renin-aldosterone system and
sympathetic nervous activity and body fluid retention but that the
vasodilative action of this peptide is attenuated in advanced CHF.
ARTICLES
Cardiorenal and neurohumoral effects of endogenous atrial natriuretic peptide in dogs with severe congestive heart failure using a specific antagonist for guanylate cyclase-coupled receptors
First Department of Internal Medicine, Shiga University of Medical Science, Ohtsu, Japan.
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