Norepinephrine stimulates apoptosis in adult rat ventricular myocytes by activation of the β-adrenergic pathway

Myocardial sympathetic activity is increased in heart failure. We tested the hypothesis that norepinephrine (NE) stimulates apoptosis in adult rat ventricular myocytes in vitro. Myocytes were exposed to NE alone (10 micromol/L), NE+propranolol (2 micromol/L), NE+prazosin (0.1 micromol/L), or isoprot...

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Bibliographic Details
Published in:Circulation (New York, N.Y.) N.Y.), 1998-09, Vol.98 (13), p.1329-1334
Main Authors: COMMUNAL, C, SINGH, K, PIMENTEL, D. R, COLUCCI, W. S
Format: Article
Language:English
Subjects:
Adenylyl Cyclases - physiology
Animals
Apoptosis - drug effects
Biological and medical sciences
Calcium Channels - physiology
Cardiology. Vascular system
Cells, Cultured
Cyclic AMP-Dependent Protein Kinases - physiology
Flow Cytometry
Heart
Heart - drug effects
Heart failure, cardiogenic pulmonary edema, cardiac enlargement
Isoproterenol - pharmacology
Male
Medical sciences
Myocardium - cytology
Norepinephrine - pharmacology
Rats
Rats, Sprague-Dawley
Receptors, Adrenergic, beta - drug effects
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Summary:Myocardial sympathetic activity is increased in heart failure. We tested the hypothesis that norepinephrine (NE) stimulates apoptosis in adult rat ventricular myocytes in vitro. Myocytes were exposed to NE alone (10 micromol/L), NE+propranolol (2 micromol/L), NE+prazosin (0.1 micromol/L), or isoproterenol (ISO, 10 micromol/L) for 24 hours. NE and ISO decreased the number of viable myocytes by approximately 35%. This effect was completely blocked by the beta-adrenergic antagonist propranolol but was not affected by the alpha1-adrenergic antagonist prazosin. NE increased DNA laddering on agarose gel electrophoresis and increased the percentage of cells that were stained by terminal deoxynucleotidyl transferase-mediated nick end-labeling from 5.8+/-1. 0% to 21.0+/-2.3% (P
ISSN:0009-7322
1524-4539
DOI:10.1161/01.CIR.98.13.1329