Publication | Closed Access
Hypoxia-induced von Willebrand factor release is blocked by verapamil.
11
Citations
0
References
1992
Year
Vwf ReleasePharmacotherapyOxidative StressInflammationMolecular PharmacologyThrombosisCalcium Antagonist VerapamilHematologyHypoxia-induced StimulationHealth SciencesVascular PharmacologyHypoxia (Medicine)Vascular BiologyPharmacologyPhysiologyEndothelial DysfunctionHemostasisClinical PharmacologyElectrophysiologyMedicineAnesthesiology
Hypoxia-induced stimulation of the rate of von Willebrand factor (vWF) release from human umbilical vein endothelial cells in culture, and the influence of the calcium antagonist verapamil, was studied using a system in which a pO2 of 20 mm Hg was achieved over 60 min. The mean +/- SEM rate of vWF release over 60 min in normoxia was 0.42 +/- 0.07% pooled plasma standard. The addition of verapamil did not alter the basal rate of vWF release, but after 60 min of hypoxia, the rate was increased to 0.71 +/- 0.03% plasma standard (p < 0.01). Verapamil at a concentration of 0.1 microgram/ml of media had no influence on the stimulated rate of release (0.78 +/- 0.07%), but increasing concentrations of verapamil up to a maximum of 1 microgram/ml attenuated the hypoxia induced stimulation (0.48 +/- 0.07%; p = 0.04 vs. hypoxic control). Thus, verapamil at this concentration completely blocked the hypoxia-induced stimulation.