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Modulation of Subcellular Ca2+ Signal by Fluid Pressure in Rat Atrial Myocytes  

Woo Sun-Hee (College of Pharmacy, Chungnam National University)
Morad Martin (Department of Pharmacology, Georgetown University Medical Center)
Publication Information
Biomolecules & Therapeutics / v.14, no.1, 2006 , pp. 19-24 More about this Journal
Abstract
Atrial chambers serve as mechanosensory systems during the haemodynamic or mechanical disturbances, which initiates arrhythmia. Atrial myocytes, lacking t-tubules, have two functionally separate sarcoplasmic reticulums (SRs): those at the periphery close to the surface membrane, and those at the cell interior (center) not associated with the membrane. To explore possible role of fluid pressure (FP) in the regulation of atrial local $Ca^{2+}$ signaling we investigated the effect of FP on subcellular $Ca^{2+}$ signals in isolated rat atrial myocytes using confocal microscopy. FP was applied to whole area of single myocyte with pressurized automatic micro-jet (200-400 $mmH_2O$) positioned close to the cell. Application of FP enhanced spontaneous occurrences of peripheral and central $Ca^{2+}$ sparks with larger effects on the peripheral release sites. Unitary properties of single sparks were not altered by FP. Exposure to higher FP often triggered longitudinal $Ca^{2+}$ wave. These results suggest that fluid pressure may directly alter excitability of atrial myocytes by activating $Ca^{2+}$-dependent ionic conductance in the peripheral membrane and by enhancing spontaneous activation of central myofilaments.
Keywords
flow pressure; atrial myocytes; $Ca^{2+}$ spark;
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