Effects of overexpression of beta2-adrenoceptor on contraction in cardiac myocytes isolated from failure hearts of rats.
- Author:
Hong SUN
1
;
Ai-min CHANG
;
Yang ZHANG
;
Xin-wei JIANG
Author Information
- Publication Type:Journal Article
- MeSH: Adenoviridae; genetics; Adrenergic beta-Antagonists; pharmacology; Animals; Cells, Cultured; Heart Failure; metabolism; physiopathology; Humans; Imidazoles; pharmacology; Isoproterenol; pharmacology; Male; Myocardial Contraction; Myocytes, Cardiac; metabolism; Rats; Rats, Sprague-Dawley; Receptors, Adrenergic, beta-2; genetics; metabolism
- From: Chinese Journal of Applied Physiology 2007;23(4):410-414
- CountryChina
- Language:Chinese
-
Abstract:
AIMTo investigate the role of overexpression of beta2-adrenoceptor on contraction in cardiac myocytes isolated from failure hearts of rats and primarily analyses its mechanisms.
METHODSPrimarily cultured cardiac myocytes were infected with adenovirus containing the sequence for human beta2-adrenoceptors. The expression of beta2-adrenoceptors was tested by Western blot. The contraction amplitudes induced by isoprenaline stimulation were measured.
RESULTSOverexpression of beta2-adrenoceptor increased the content in failure cardiac myocytes. The contraction amplitudes in failure cardiac myocytes were lower than that in the control (P < 0.01). Overexpression of beta2 adrenoceptor improved the contraction of failure cardiac myocytes (P < 0.01, Failure+ Adv.Beta2 group vs. Failure group). Selective beta2-adrenoceptor antagonist ICI 118,551 partially reversed the effects (P < 0.05, Failure+ Adv.beta2 + ICI group vs Failure + Adv.beta2 group), but the contraction amplitudes in this Failure +/- Adv.beta2 + ICI 118,551 group were still higher than that in only heart failure group (P < 0.05). Selective beta1 adrenoceptor antagonist CGP20712A completely inhibited the effects of overexpression of beta2 adrenoceptor on contraction amplitude in failure cardiac myocytes.
CONCLUSIONOverexpression of beta2-adrenoceptors improves the contraction of cardiac myocytes isolated from failure hearts of rats. The effect is related to beta1-adrenoceptor.
