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

The anti‐aggregating properties of vascular endothelium: interactions between prostacyclin and... 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. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png British Journal of Pharmacology Wiley

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

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Publisher
Wiley
Copyright
1987 British Pharmacological Society
ISSN
0007-1188
eISSN
1476-5381
D.O.I.
10.1111/j.1476-5381.1987.tb11367.x
Publisher site
See Article on Publisher Site

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.

Journal

British Journal of PharmacologyWiley

Published: Nov 1, 1987

References

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