Enhancement of Ca(2+) transients and contraction of single ventricular myocytes of rats by 5-(N,N-dimethyl) amiloride.
- Author:
Xiang-Li CUI
1
;
Huan-Zhen CHEN
;
Dong-Mei WU
;
Bo-Wei WU
Author Information
1. Department of Physiology, Shanxi Medical University, Taiyuan 030001, China. wubowei@public.ty.sx.cn
- Publication Type:Journal Article
- MeSH:
Amiloride;
analogs & derivatives;
pharmacology;
Animals;
Calcium;
metabolism;
Cardiomyopathy, Hypertrophic;
drug therapy;
Heart Ventricles;
cytology;
Myocardial Contraction;
drug effects;
Myocytes, Cardiac;
metabolism;
Rats;
Rats, Wistar;
Sodium-Calcium Exchanger;
antagonists & inhibitors;
pharmacology
- From:
Acta Physiologica Sinica
2002;54(3):219-224
- CountryChina
- Language:English
-
Abstract:
The effects of 5-(N,N-dimethyl)amiloride (DMA) (a blocker of Na(+)/H(+) exchanger or Na(+)/Ca(2+) exchanger) on calcium transient and cell contraction in isolated ventricular myocytes in normal rats and rats with myocardial hypertrophy were examined using ion imaging system with a charge coupled digital camera (CCD camera). Loading myocytes with Fura-2, electrically triggered Ca(2+) transients and cell shortening were measured simultaneously. The results showed that 10 micromol/L DMA increased Ca(2+) transient and cell shortening from 209.60+/-54.96 and 3.07+/-0.97 micrometer to 238.50+/-80.41 and 4.07+/-1.02 micrometer, respectively (P<0.05), which was completely abolished by application of KB-R7943, a specific reverse mode Na(+)/Ca(2+) exchanger blocker. After blocking L-type Ca(2+) channels by nicardipine, DMA also enhanced Ca(2+) transient and cell shortening. In rats with myocardial hypertrophy, DMA showed the common pharmacologic profile as in normal rats but more intense stimulating effects on Ca(2+) transient and cell contraction. The results suggest that DMA increase Ca(2+) transient and cell contraction via stimulating reverse mode Na(+)/ Ca(2+) exchange, and the stimulating effect is more pronounced in rats with myocardial hypertrophy than in normal ones.
