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Articles in PresS, published online ahead of print September 27, 2001
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00319.2001
Submitted on April 19, 2001
Accepted on September 18, 2001
1 Cardiology Unit, Department of Medicine, University of Rochester Medical Center, Rochester, NY, USA
* To whom correspondence should be addressed. E-mail: Chang-seng_Liang{at}urmc.rochester.edu.
Sympathetic neurotransmitters are diminished in cardiac sympathetic efferent nerve endings in congestive heart failure (CHF). Similar changes occur after exogenous NE infusion. Recently, NE has been shown to reduce nerve growth factor (NGF) in cultured myocytes. Since NGF plays an important role in the survival of sympathetic neurons through high-affinity neurotrophic receptor tyrosine kinase (TrKA), we speculate that the loss of noradrenergic transmitters in the failing heart may be caused by the NE-mediated reduction of NGF or TrKA. Adult mongrel dogs were assigned to receive either a rapid ventricular pacing (225 beats/min) or NE (0.5 µg/kg/min) minipump for 8 weeks. The control animals received either a cardiac pacing of 100 beats/min or saline infusion. We measured NGF and TrKA protein expression by Western blot and immunocytochemistry, NGF and TrkA mRNA expression by RT-PCR, neuronal catecholaminergic histofluorescence and tyrosine hydroxylase immunostained profiles, and plasma NE. Rapid ventricular pacing produced CHF with increased plasma NE, decreased myocardial protein expression of NGF (0.61±0.07 vs. 1.04±0.04, p<0.05), and TrKA (0.75±0.08 vs. 0.98±0.06, p<0.05), mRNA expression of NGF and TrKA, and reduced neuronal catecholaminergic (197±23 vs. 485±43, p<0.05) and tyrosine hydroxylase immunostained (360±51 vs. 773±76, p<0.05) profiles. A decrease in tissue NGF or TrKA protein was also found by immunocytochemistry. Similar changes occurred in NE-treated animals. Tissue NGF and TrKA levels correlated closely with the noradrenergic transmitter profiles. We conclude that cardiac NGF and TrKA are reduced by rapid ventricular pacing and NE infusion, and that these changes correlate with the decreases of cardiac catecholaminergic and tyrosine hydroxylase profiles. The findings indicate that the decrease of cardiac sympathetic neurotransmitters in heart failure is associated with NE-mediated reduction of NGF and TrKA.
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