[Expression of beta2-adrenergic receptor and its effect on the proliferation of neonatal rat cardiac fibroblasts].

Sheng Li Xue Bao

Institute of Vascular Medicine, Peking University Third Hospital, The Reference Laboratory of Ministry of Education for Molecular Cardiovasology, Beijing 100083.

Published: June 2003

AI Article Synopsis

  • The study examined the expression of beta-adrenergic receptor subtypes in neonatal rat cardiac fibroblasts and how it influences their proliferation.
  • There were no significant differences found in the density or affinity of beta-adrenergic receptors between cardiomyocytes and cardiac fibroblasts.
  • The findings indicated that the proliferation of cardiac fibroblasts induced by isoproterenol is mainly mediated by the beta(2)-adrenergic receptor, as confirmed by the effects of different antagonists.

Article Abstract

The expression of beta-adrenergic receptor subtypes and its effect on neonatal rat cardiac fibroblast proliferation were investigated by radioligand binding assay and [(3)H]-thymidine incorporation analysis, respectively. The results indicated that there was no significant difference in the beta-adrenergic receptor density (B(max)) and affinity (K(D)) between cardiomyocytes and cardiac fibroblasts. The [(125)I]-pindolol competitive inhibition curves (ICI 118551 and CGP 20712A) were significantly better fit in a one-site model in membrane preparation of cardiac fibroblasts. In cultured cardiac fibroblasts, 0.1 micromol/L isoproterenol-induced [(3)H]-thymidine incorporation was completely inhibited by a selective beta (2)-AR antagonist ICI 118551, or a non-selective beta-AR antagonist propranolol, but not by CGP 20712A, a selective beta(1)-AR antagonist. These results suggest that isoproterenol-induced cardiac fibroblast proliferation is mediated by beta(2)-AR, the preponderant beta-AR subtype in cardiac fibroblasts.

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