Effect of @entity5261 on intracellular free @entity460 concentration in isolated XXXX ventricular myocytes.

@entity35 @entity3576 @entity2647 @entity5261 @entity460 @entity141 @entity9898 @entity4338
The present study was to investigate the effects of @entity5261 (Agm) on free intracellular @entity460 concentration ([ @entity141 ]( i )) of isolated @entity35 ventricular myocytes. [ @entity141 ]( i ) was measured by confocal microscopy in single @entity35 ventricular myocytes which were dissociated by enzymatic dissociation method and loaded with @entity3576 . The changes in [ @entity141 ]( i ) were represented by fluorescence intensity (FI) or relative fluorescence intensity (F/F(0)%). The results showed that the control level of FI value of single @entity35 ventricular myocytes was 128.8+/-13.8 and 119.6+/-13.6 in the presence of normal Tyrode's solution containing @entity141 1.0 mmol/L and @entity141 -free Tyrode's solution, respectively. There was no difference between these two groups (P>0.05). Agm 0.1, 1, and 10 mmol/L significantly reduced the [ @entity141 ]( i ) in both extracellular solutions in a concentration-dependent manner. The similar effect of Agm on [ @entity141 ]( i ) was also observed in the presence of EGTA 3 mmol/L. KCl 60 mmol/L, PE 30 micromol/L, and @entity9898 10 micromol/L, all these substances induced [ @entity141 ]( i ) elevations in ventricular myocytes. Agm (0.1, 1, and 10 mmol/L) markedly inhibited the increase in [ @entity141 ]( i ) induced by @entity4338 , @entity2647 (PE), and @entity9898 . When @entity141 waves were produced by increasing extracellular @entity141 concentration from 1 to 10 mmol/L, 1 mmol/L Agm could block the propagating waves of elevated [ @entity141 ]( i ), and reduce the velocity and duration of propagating waves. These results suggest that Agm possesses an inhibitory effects on [ @entity141 ]( i ) via blocking voltage-dependent @entity141 channel, and possibly by alleviating @entity460 release from SR in single isolated @entity35 ventricular myocytes.
