CHANGES OF ATRIAL-NATRIURETIC-PEPTIDE IN BRAIN-AREAS OF RATS WITH CHRONIC MYOCARDIAL-INFARCTION

We measured immunoreactive atrial natriuretic peptide (ANP) in 18 sele cted, microdissected brain areas. Rats were studied 8 wk. after corona ry ligation or sham operation or as nonoperated control animals. In se parate animals, hemodynamic and plasma parameters were measured. Rats with myocardial infarction had marked elevated right atrial and left v entricular end-diastolic pressure (2.6 +/- 0.6 and 16.2 +/- 3.1 mmHg, respectively; n = 15) vs. sham-operated rats (1.3 +/- 1.0 and 5.5 +/- 1.2 mmHg, n = 14; P < 0.05) and depressed maximal rate of pressure dev elopment (9,613 +/- 980 vs. 15,600 +/- 2,027 mmHg/s; P < 0.05) but sim ilar arterial pressure (126 +/- 4 vs. 124 +/- 3 mmHg; P > 0.05). After myocardial infarction (n = 10), plasma ANP, renin activity, and angio tensin (ANG) II were elevated (53.1 +/- 16.2 pg/ml, 10.7 +/- 2.5 ng AN G I . ml(-1). h(-1), and 219.6 +/- 11.0 fmol/ml, respectively) vs. sha m rats (12.0 +/- 2.2 pg/ml, 5.7 +/- 0.7 ng ANG I . ml(-1). h(-1), and 142.9 +/- 9.4 fmol/ml; n = 10; P < 0.05), whereas vasopressin and aldo sterone levels remained unchanged among groups. In rats with myocardia l infarction, a substantial decrease of ANP was found in the medial pr eoptic nucleus, the supraoptic nucleus, the subfornical organ, the par aventricular nucleus, and the locus ceruleus. These nuclei are involve d 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 u nclear. However, the data suggest that myocardial infarction and chron ic left ventricular dysfunction may induce changes of a neurotransmitt er in brain.