Expression of beta2-adrenergic receptor and its effect on the proliferation of neonatal rat cardiac fibroblasts.
- Author:
Feng YIN
1
;
Zhi-Zhen LU
;
Qi-De HAN
;
You-Yi ZHANG
Author Information
1. Institute of Vascular Medicine, Peking University Third Hospital, The Reference Laboratory of Ministry of Education for Molecular Cardiovasology, Beijing 100083.
- Publication Type:Journal Article
- MeSH:
Animals;
Animals, Newborn;
Cell Proliferation;
Cells, Cultured;
Fibroblasts;
cytology;
metabolism;
Myocytes, Cardiac;
cytology;
metabolism;
Rats;
Rats, Wistar;
Receptors, Adrenergic, beta-2;
genetics;
metabolism;
physiology
- From:
Acta Physiologica Sinica
2003;55(3):251-254
- CountryChina
- Language:Chinese
-
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.
