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-Adrenergic stimulation causes cardiocyte apoptosis:
influence of tachycardia and hypertrophy
1 Division of Cardiology and Departments of 2 Pathology and 3 Cell Biology, Albert Einstein College of Medicine, Bronx, New York 10461
To establish
whether catecholamines per se in the absence of significant increases
in systolic load induce myocardial damage via apoptosis, rats were
treated with vehicle or isoproterenol (400 µg · kg
1 · h1).
Apoptotic cardiocytes (Apo) were identified in paraffin-embedded sections using terminal deoxynucleotide transferase-mediated dUTP nick
end labeling. Results were confirmed using an independent ligase assay.
Systolic blood pressures were comparable in isoproterenol-treated and
control rats. Twenty-four hours of treatment with isoproterenol resulted in significant numbers of Apo compared with control [7.9 ± 2.5 vs. 0.3 ± 0.3 (SE)
cm2,
P < 0.05]. A cohort of animals
was subjected to ventricular pacing to induce a tachycardia equivalent
to that induced by isoproterenol, and these animals did not show an
increase in Apo. The left ventricular hypertrophy induced by 2 wk of
abdominal aortic banding also increased Apo (~7.2-fold); however, 24 h of isoproterenol infusion did not induce additional Apo in these
rats. Thus catecholamines, in the absence of altered systolic load,
induce Apo which is not mediated solely by tachycardia. Left
ventricular hypertrophy secondary to abdominal aortic banding is
associated with Apo, but this does not increase sensitivity to
isoproterenol-induced Apo.
catecholamines; myocardial cell death; cardiac pacing; ligase reaction; rats
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