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Effect of Fluid Pressure on L-type $Ca^{2+}$ Current in Rat Ventricular Myocytes  

Lee Sun-Woo (College of Pharmacy, Chungnam National University)
Woo Sun-Hee (College of Pharmacy, Chungnam National University)
Publication Information
YAKHAK HOEJI / v.50, no.2, 2006 , pp. 111-117 More about this Journal
Abstract
Cardiac chambers serve as mechanosensory systems during the haemodynamic or mechanical disturbances. To examine a possible role of fluid pressure (FP) in the regulatien of atrial $Ca^{2+}$ signaling we investigated the effect of FP on L-type $Ca^{2+}$ current $(I_{Ca})$ in rat ventricular myocytes using whole-cell patch-clamp technique. FP $(\sim40cm\;H_2O)$ was applied to whole area of single myocytes with electronically controlled micro-jet system. FP suppressed the magnitude of peak $I_{Ca}$ by $\cong25\%$ at 0 mV without changing voltage dependence of the current-voltage relationship. FP significantly accelerated slow component in inactivation of $I_{Ca}$, but not its fast component. Analysis of steady-state inactivation curve revealed a reduction of the number of $Ca^{2+}$ channels available for activity in the presence of FP. Dialysis of myocytes with high concentration of immobile $Ca^{2+}$ buffer partially attenuated the FP-induced suppression of $I_{Ca}$. In addition, the intracellular $Ca^{2+}$ buttering abolished the FP-induced acceleration of slow component in $I_{Ca}$ inactivation. These results indicate that FP sup-presses $Ca^{2+}$ currents, in part, by increasing cytosolic $Ca^{2+}$ concentration.
Keywords
fluid pressure (FP); L-type $Ca^{2+}$ current ($I_{Ca}$); ventricular myocytes; whole-cell patch clamp; $Ca^{2+}$ buffer;
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