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Articles in PresS, published online ahead of print June 27, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.01131.2001
Submitted on December 30, 2001
Accepted on June 14, 2002
1 Medicine, University of Rochester Medical Center, Rochester, NY, USA
2 Neurobiology and Anatomy, University of Rochester Medical Center, Rochester, NY, USA
* To whom correspondence should be addressed. E-mail: Chang-seng_Liang{at}urmc.rochester.edu.
Right heart failure (RHF) is characterized by chamber-specific reductions of myocardial norepinephrine (NE) reuptake, ß-receptor density, and profiles of cardiac sympathetic nerve ending neurotransmitters. To study the functional linkage between NE uptake and the pre- and post-synaptic changes, we administered desipramine (225 mg/day), a NE uptake inhibitor, to dogs with RHF produced by tricuspid avulsion and progressive pulmonary constriction or sham-operated dogs for 6 weeks. Animals receiving no desipramine were studied as control. We measured myocardial NE uptake activity using [3H]NE,ß-receptor density by [125I]iodocyanopindolol, inotropic responses to dobutamine, and noradrenergic terminal neurotransmitter profiles by glyoxylic acid induced histofluorescence for catecholamines, and immunocytochemical staining for tyrosine hydroxylase and neuropeptide Y. Desipramine decreased myocardial NE uptake activity, and had no effects on the resting hemodynamics in both RHF and sham animals, but decreased ß-adrenoceptor density and ß-adrenergic inotropic responses in both ventricles of the RHF animals. However, desipramine treatment prevented the reduction of sympathetic neurotransmitter profiles in the failing heart. Our results indicate that NE uptake inhibition facilitates the reduction of myocardial ß-adrenoceptor density and ß-adrenergic subsensitivity in RHF, probably by increasing interstitial NE concentrations, but protect the cardiac noradrenergic nerve endings from damage, probably via blockade of NE-derived neurotoxic metabolites into the nerve endings.
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