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Cardiovascular Research 1998 38(2):522-530; doi:10.1016/S0008-6363(98)00040-6
© 1998 by European Society of Cardiology
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Copyright © 1998, European Society of Cardiology

Downregulation of β-adrenergic receptors by low density lipoproteins and its prevention by β-adrenergic receptor antagonists

Bernhard R Brehma,*, Matthias Meergansa, Dorothea I Axela, Martin Pfohlc, Helmut Heinleb and Karl R Karscha

aDepartment of Cardiology, University of Tübingen, Otfried-Müllerstrasse 10, D-72076 Tübingen, Germany
bInstitute of Physiology, University of Tübingen, Tübingen, Germany
cDepartment of Endocrinology, University of Tübingen, Tübingen, Germany

* Corresponding author. Tel.: +49 (7071) 298-2711; Fax: +49 (7071) 360245; E-mail: 101566.341@compuserve.com

Objective: Vasodilation by β-adrenergic receptors of smooth muscle cells appears to be impaired early after the onset of hypercholesteremia. The aim of this study was to analyze the modulation of β-adrenergic receptor density and adenylyl cyclase activity in the presence of moderately elevated concentrations of LDL. The effects of β1- and β2-adrenergic receptor antagonists on LDL-induced receptor changes were studied. Methods and results: Media explants of porcine coronary arteries were incubated with moderately elevated LDL concentrations (0.7–3.9 mmol/l). The density of β-adrenergic receptors was determined in plasma membranes using the radioligand [125I]iodocyanopindolol. LDL (3.9 mmol/l) resulted in a decrease of β-adrenergic receptor density (control 137±5 vs. 89±7 fmol/mg protein, P<0.01). After removal of LDL and cultivation for an additional 3 days β-adrenergic receptors increased to 129±5 fmol/mg. In the presence of the β1- or β2-adrenergic receptor antagonists the LDL-mediated decrease was inhibited. Addition of metoprolol after 3 days of LDL incubation caused a restoration of receptor density. The basal, isoproterenol- and forskolin-stimulated adenylyl cyclase activities were increased after LDL incubation by 180, 110 or 80%, respectively. Conclusion: Moderately elevated LDL levels decreased β-adrenergic receptor density while adenylyl cyclase activity was simultaneously increased. β1- or β2-adrenergic receptor antagonists prevented this receptor decrease and might preserve the β-adrenergic receptor density in the presence of moderately elevated LDL levels.

KEYWORDS Moderately elevated LDL; Porcine coronary artery; β-Adrenergic receptor; β-Blockade; Adenylyl cyclase


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