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Research Article Free access | 10.1172/JCI114294

Decreased adrenergic neuronal uptake activity in experimental right heart failure. A chamber-specific contributor to beta-adrenoceptor downregulation.

C S Liang, T H Fan, J T Sullebarger, and S Sakamoto

Cardiology Unit, University of Rochester Medical Center, New York 14642.

Find articles by Liang, C. in: JCI | PubMed | Google Scholar

Cardiology Unit, University of Rochester Medical Center, New York 14642.

Find articles by Fan, T. in: JCI | PubMed | Google Scholar

Cardiology Unit, University of Rochester Medical Center, New York 14642.

Find articles by Sullebarger, J. in: JCI | PubMed | Google Scholar

Cardiology Unit, University of Rochester Medical Center, New York 14642.

Find articles by Sakamoto, S. in: JCI | PubMed | Google Scholar

Published October 1, 1989 - More info

Published in Volume 84, Issue 4 on October 1, 1989
J Clin Invest. 1989;84(4):1267–1275. https://doi.org/10.1172/JCI114294.
© 1989 The American Society for Clinical Investigation
Published October 1, 1989 - Version history
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Abstract

The reduction of myocardial beta-adrenoceptor density in congestive heart failure has been thought to be caused by agonist-induced homologous desensitization. However, recent evidence suggests that excessive adrenergic stimulation may not produce myocardial beta-receptor downregulation unless there is an additional defect in the local norepinephrine (NE) uptake mechanism. To investigate the association between beta-adrenoceptor regulation and NE uptake activity, we carried out studies in 30 dogs with right heart failure (RHF) produced by tricuspid avulsion and progressive pulmonary artery constriction and 23 sham-operated control dogs. We determined NE uptake activity by measuring accumulation of [3H]NE in tissue slices, NE uptake-1 carrier density by [3H]mazindol binding and beta-adrenoceptor density by [3H]dihydroalprenolol binding. Compared with sham-operated dogs, RHF dogs showed a 26% decrease in beta-adrenoceptor density, a 51% reduction in NE uptake activity, and a 57% decrease in NE uptake-1 carrier density in their right ventricles. In addition, right ventricle beta-receptor density correlated significantly with NE uptake activity and NE uptake-1 carrier density. In contrast, neither NE uptake activity nor beta-receptor density in the left ventricle and renal cortex was affected by RHF. Thus, the failing myocardium is associated with an organ- and chamber-specific subnormal neuronal NE uptake. This chamber-specific loss of NE uptake-1 carrier could effectively reduce local NE clearance, and represent a local factor that predisposes the failing ventricle to beta-adrenoceptor downregulation.

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