Circulation, Vol 79, 620-633, Copyright © 1989 by American Heart Association
H Drexler, J Hanze, M Finckh, W Lu, H Just and RE Lang
This study examined the relation between synthesis, atrial storage, and
plasma levels of atrial natriuretic peptide (ANP), and it examined plasma
ANP levels and hemodynamic output in response to volume expansion in a rat
model of myocardial infarction and failure. Arterial ANP concentrations did
not correlate linearly with infarct size, but they did show an abrupt
increase when infarct size exceeded 30% of the left ventricle, similar to
the abrupt increase of left ventricular end- diastolic pressure with
infarct size greater than 30%. Consequently, a close relation was found
between plasma ANP levels and left ventricular end-diastolic pressure (n =
23, r = 0.89, p less than 0.001). Atrial ANP content per gram of tissue but
not ANP content per pair of atria was reduced in rats with large infarcts
(greater than 40%, p less than 0.05 vs. control animals). ANP mRNA level
per pair of atria (related to total atrial RNA), determined by liquid
hybridization (controlled by northern blot analysis), was increased by 38%
in infarcted rats (p less than 0.05 vs. controls), but the ratio of atrial
ANP mRNA relative to atrial beta-actin mRNA levels was not increased. Right
and left ventricular ANP mRNA level increased by 90% and 380%,
respectively, far exceeding the concomitant increase in beta-actin mRNA
(+26% in the left ventricle). Plasma ANP increased with volume loading in
controls and rats with moderate infarcts but not in rats with large
infarcts despite a similar increase in right atrial pressure (compared with
control animals); thus, the relation of delta ANP/delta right atrial
pressure exerted by volume loading decreased in rats with large infarcts.
Similarly, the response of cardiac output and renal blood flow (determined
by radioactive microspheres) to volume loading was attenuated in rats with
large infarcts. Thus, in this model of chronic cardiac failure, the
activation of the ANP system is closely coupled with the increase in
intracardiac pressures without correlating linearly to the extent of
myocardial loss. Second, in severe cardiac failure, additional stimulation
such as volume loading may elicit only an attenuated ANP secretion
response, for example, due to saturation of the ANP receptor sensing system
or to a limited transformation rate of pro-ANP. Third, the increase in
atrial ANP synthesis and the increase in atrial ANP gene expression seems
limited; however, substantial specific ANP gene expression occurs in the
ventricles, which, in turn, may contribute to increased plasma ANP levels
in chronic heart failure.
ARTICLES
Atrial natriuretic peptide in a rat model of cardiac failure. Atrial and ventricular mRNA, atrial content, plasma levels, and effect of volume loading
Medizinische Klinik III, University of Freiburg, FRG.
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