Direct evidence for the contractile capacity of endothelial cells
Faculty of Pharmaceutical, Biomedical and Veterinary Sciences. Pharmacy
New York, N.Y.
Thrombosis research. - New York, N.Y.
, p. 505-520
Dog aorta-derived endothelial cells, grown in culture and resuspended in normal human or canine citrated platelet-free plasma, invariably retracted the fibrin clot when stimulated with exogenously added or endogenously formed thrombin. The onset, rate and extent of this retraction depended upon the cell density, the concentration of thrombin, the cellular integrity, the homogeneous cell distribution and the availability of free extracellular Ca2+. Endothelial cell-induced clot retraction was completely inhibited by EGTA, by VK 774-induced phosphodiesterase inhibition and by combined treatment with PGE1 and papaverine. It was partly reduced by nocodazole-induced microtubule disruption, by cytochalasin B, by verapamil- and flunarizine-induced blockade of Ca2+-fluxes but was not affected by cyclo-oxygenase inhibitor suprofen. Incorporation of additional Ca2+ into non-retracting, Reptilase®-formed clots resulted in a retraction which was not blocked by heparin. In addition of 5-hydroxytryptamine, ADP, histamine or epinephrine slightly enhanced this retraction.