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Effects of allicin on angiotensin Ⅱ-induced calcium current and intracellular free calcium concentration in human atrial myocytes / 中国组织工程研究
Article in Chinese | WPRIM (Western Pacific) | ID: wpr-409442
Responsible library: WPRO
ABSTRACT

BACKGROUND:

Angiotensin Ⅱ has been found to induce atrial electrical remodeling, which can be blocked or inhibited by allicin.

OBJECTIVE:

To study the effects of allicin on angiotensin Ⅱ-induced calcium channel current and intracellular free calcium concentration in human atrial myocytes.

DESIGN:

A randomized controlled study based on human atrial myocytes freshly isolated.

SETTING:

Cardiology department of a military medical university of Chinese PLA.

METHODS:

This study was carried out from June 2003 to June 2004 in the Laboratory of Cardiology Department, Xijing Hospital, the Fourth Military Medical University of Chinese PLA. Ten patients with congenital heart disease who underwent extracorporeal circulation surgery were included in the study. Among them, there were 6 males and 4 females with the average age of 15 ± 6 years. Tissue samples were taken from their right auricle and sent to the lab, where the atrial myocytes were freshly isolated. There were four co-administration of angiotensin Ⅱ (0. 1 μmol/L)and allicin(50 μmol/L).The conventional whole-cell configuration of the patch-clamp technique was used to detect membrane electric current of Ca2 + in L type. Confocal microscope was used with Fluo-3/AM as calcium indicator to detect changes of intracellular free calcium concentration immediately and 15 minutes after drug intervention, respectively.MAIN OUTCOME

MEASURES:

The peak density of electric current of Ca2 + in L type and alteration of fluoresence intensity of intracellular free calcium concentration.electric current of Ca2 + in L type in human atrial myocytes was significantly increased by angiotensin Ⅱ of 0. 1 μmol/L[( - 12. 77 ± 1. 61) vs ( -5.78affect electric current of Ca2+ in L type in human atrial myocytes group, the peak density of electric current of Ca2 + in L type was significantly lower than that in angiotensin Ⅱ group[ ( - 8.75 ± 0.97) pA/pF, P < 0. 05 ].in angiotensin Ⅱ group was significantly higher than that in control and allicin groups[(2 610.1±112.6, (299.2±27.3)%; 653.9±42.5, 0;simultaneously with angiotensin Ⅱ, the alteration of intracellular fluoresence intensity was much lower than that in angiotensin Ⅱ group[ ( 1284.9 ± 85.2,(96.5±8.4)%;P <0.05].

CONCLUSION:

Allicin antagonizes angiotensin Ⅱ-induced increase in the peak density of electric current of Ca2+ in L type and intracellular calcium overload, which may relieve atrial electrical remodeling.
Full text: Available Database: WPRIM (Western Pacific) Type of study: Controlled clinical trial Language: Chinese Journal: Chinese Journal of Tissue Engineering Research Year: 2005 Document type: Article
Full text: Available Database: WPRIM (Western Pacific) Type of study: Controlled clinical trial Language: Chinese Journal: Chinese Journal of Tissue Engineering Research Year: 2005 Document type: Article
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