Àá½Ã¸¸ ±â´Ù·Á ÁÖ¼¼¿ä. ·ÎµùÁßÀÔ´Ï´Ù.
KMID : 0370220110550030247
Yakhak Hoeji
2011 Volume.55 No. 3 p.247 ~ p.250
Decrease of Intracellular pH and Activation of Na+¤ÑH+ Exchanger by Fluid Pressure in Rat Ventricular Myocytes
Kim Joon-Chul

Woo Sun-Hee
Abstract
An increase in ventricular pressure can alter cardiac excitation and contraction. Recent report has demonstrated that fluid pressure (FP) suppresses L-type Ca©÷+ current with acceleration of the current inactivation in ventricular myocytes. Since the L-type Ca©÷+ channels known to be regulated by intracellular pH (pH©û), this study was designed to explore whether pressurized fluid flow affects pHi in isolated rat ventricular myocytes. A flow of pressurized (~16 dyne/cm©÷) fluid, identical to that bathing the myocytes, was applied onto single myocytes, and intracellular H+ concentration was monitored using confocal H+ imaging. FP significantly decreased pH©û by 0.07¡¾0.01 pH units (n=16, P<0.01). Intracellular acidosis enhances the activity of Na+¤ÑH+ exchanger (NHE). Therefore, we examined if the NHE activity is increased by FP using the NHE inhibitor, HOE642. Although HOE642 did not alter pH©û in control conditions, it decreased pH©û in cells pre-exposed to FP, suggesting enhancement of NHE activity by FP. In addition, FP-induced intracellular acidosis was larger in cells pre-treated with HOE642 than in cells under the control conditions. These results suggest that FP induces intracellular acidosis and that NHE may contribute to extrude H+ during the FP-induced acidosis in rat ventricular myocytes.
KEYWORD
fluid pressure, intracellular pH, ventricular myocytes, Na+¤ÑH+ exchanger, HOE642
FullTexts / Linksout information
Listed journal information
ÇмúÁøÈïÀç´Ü(KCI)