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KMID : 0811720070110000076
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Korean Journal of Physiology & Pharmacology
2007 Volume.11 No. 0 p.76 ~ p.0
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Fluid Pressure Modulates L-type Ca2+ Channel via Enhancement of Ca2+-induced Ca2+ Release in Rat Ventricular Myocytes
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Lee Sun-woo
Kim Joon-Chul
Woo Sun-Hee
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Abstract
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This study examines whether fluid pressure (FP) modulates the L-type Ca2+ channel in cardiomyocytes, and investigates the underlying cellular mechanism(s) involved. A flow of pressurized (~16 dyne/cm2) fluid, identical to that bathing the myocytes, was applied onto single isolated rat ventricular myocytes using a micro-perfusion method. The Ca2+ current (ICa) and cytosolic Ca2+ signals were measured using a whole-cell patch-clamp and confocal Ca2+ imaging, respectively. It was found that the FP reversibly suppressed ICa (by 25% at ~16 dyne/cm2) without altering the voltage dependence of the current-voltage relationships, and that the level of suppression depended on the level of pressure. The FP accelerated the inactivation of ICa and elicited a hyperpolarizing shift of the steady-state inactivation curve of ICa. The effects of the FP on the magnitude and inactivation of ICa were resistant to the stretch-activated channel inhibitor streptomycin. Interestingly, the Ba2+ current through the Ca2+ channel was only slightly decreased by the FP (5% at ~16 dyne/cm2), suggesting a Ca2+ influx-dependent, indirect inhibition of the Ca2+ channel during FP stimulation. The magnitudes of cytosolic Ca2+ transients and the basal Ca2+ level in field-stimulated ventricular myocytes were significantly increased by the FP. Dialysis of myocytes with high concentrations of BAPTA, the Ca2+ buffer, eliminated the FP-induced acceleration of ICa inactivation and reduced the inhibitory effect of the FP on ICa by 80%. These results suggest that the fluid pressure indirectly suppresses the Ca2+ channel by enhancing the Ca2+ current-triggered intracellular Ca2+ release in rat ventricular myocytes.
Source: Korean Journal of Physiology & Pharmacology.2007 Oct;11(Suppl II):S76-S76
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KEYWORD
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L-type Ca2+ current, Fluid pressure, Ventricular myocytes, Cytosolic Ca2+ transient
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