Changes of atrial natriuretic peptide in brain areas of rats with
chronic myocardial infarction.
Hu, Kai, Peter Gaudron, Udo Bahner, Miklos Palkovits, Georg Ertl.
Department of Medicine, W[umlaut]urzburg University, 97080
W[umlaut]urzburg, Germany, First Department of Anatomy, Semmelweis
University, Medical School, H-1450 Budapest, Hungary
APStracts 2:0305H, 1995.
We measured immunoreactive ANP in 18 selected, microdissected brain
areas. Rats were studied 8 weeks after coronary ligation, sham
operation or as non-operated control animals. In separate animals,
hemodynamic and plasma parameters were measured. Rats with myocardial
infarction had marked elevated right atrial and left ventricular end
-diastolic pressure (2.6+/-0.6, 16.2+/-3.1 mmHg, n=15) vs. sham rats
(1.3+/-1.0, 5.5+/-1.2 mmHg, n=14; p<0.05), and depressed
dp/dtmax (9613+/-980 vs. 15600+/-2027 mmHg/s; p<0.05) but
similar arterial pressure (126+/-4 vs. 124+/-3 mmHg; p>0.05).
Post myocardial infarction (n=10), plasma ANP, renin activity and
angiotensin II were elevated (53.1+/-16.2 pg/ml, 10.7+/-2.5 ng
AI/ml/hr, 219.6+/-11.0 fmol/ml) vs. sham rats (12.0+/-2.2, 5.7+/-0.7,
142.9+/-9.4; n=10; p<0.05), while vasopressin and aldosterone
levels remained unchanged among groups. In rats with myocardial
infarction, a substantial decrease of ANP was found in the medial
preoptic nucleus, in the supraoptic nucleus, in the subfornical
organ, in the paraventricular nucleus and in the locus coeruleus.
These nuclei are involved in electrolyte and fluid homeostasis, blood
pressure regulation and modulation of neuroendocrine systems. The
mechanism of this reduction and the consequences for systemic
adaption or decompensation remain unclear. However, the data suggest
that myocardial infarction and chronic left ventricular dysfunction
may induce changes of a neurotransmitter in brain.
Received 26 September 1994; accepted in final form 13 July 1995.
APS Manuscript Number H866-4.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 30 July 1995.