Shear stress enhances prostacyclin release from endocardial endothelial cells.

Abstract The effect of shear stress on the release of prostacyclin (PGI 2 ) from cultured endocardial endothelial cells (EECs) was investigated. EECs were harvested from the right ventricle (RV) and the left ventricle (LV) of porcine heart. Confluent EECs were incubated under various degrees of shear stress (0.2, 1, 4 and 6 dyne/cm 2 ) and PGI 2 release from each cell was measured. PGI 2 release from LV-EECs and RV-EECs was enhanced by the elevation of shear stress in a shear-dependent manner with a rapid increase at the onset of flow; however, there was no significant difference in PGI 2 production between RV-EECs and LV-EECs. production of PGI 2 was significantly inhibited from cells exposed to 8-(dimetilamino) octyl 3,4,5-trymrthoxybenzoate hydrochloride (10 and 100 μM: an inhibitor of intracellular calcium mobilization) or cyclopiazonic acid (10 μM: an endoplasmic reticulum Ca 2+ -ATPase inhibitor). These results indicate that shear stress enhances PGI 2 release from cultured EECs and that mechanotransduction of shear stress depends on calcium mobilization in EECs.