The anti‐aggregating properties of vascular endothelium: interactions between prostacyclin and nitric oxide

Abstract

1 The interactions between endothelium-derived nitric oxide (NO) and prostacyclin as inhibitors of platelet aggregation were examined. 2 Porcine aortic endothelial cells treated with indomethacin and stimulated with bradykinin (10–100 nm) released NO in quantities sufficient to account for the inhibition of platelet aggregation attributed to endothelium-derived relaxing factor (EDRF). 3 In the absence of indomethacin, stimulation of the cells with bradykinin (1–3 nm) released small amounts of prostacyclin and EDRF which synergistically inhibited platelet aggregation. 4 EDRF and authentic NO also caused disaggregation of platelets aggregated either with collagen or with U46619. 5 A reciprocal potentiation of both the anti-and the dis-aggregating activity was also observed between low concentrations of prostacyclin and authentic NO or EDRF released from endothelial cells. 6 It is likely that interactions between prostacyclin and NO released by the endothelium play a role in the homeostatic regulation of platelet-vessel wall interactions.