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Interactions of iloprost and sodium nitroprusside on vascular smooth muscle and platelet aggregation
Author(s) -
Lidbury Paul S.,
Antunes Edson,
Nucci Gilberto,
Vane John R.
Publication year - 1989
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1989.tb12674.x
Subject(s) - iloprost , sodium nitroprusside , vascular smooth muscle , platelet aggregation , chemistry , platelet , pharmacology , medicine , cardiology , smooth muscle , prostacyclin , nitric oxide
1 The aim of the study was to assess and quantify any synergism occuring between the stable analogues of prostacyclin (iloprost) and nitric oxide (sodium nitroprusside) with respect to both relaxation of vascular smooth muscle and inhibition of platelet aggregation in the rabbit. 2 Iloprost (0.3–3 ng ml −1 ) and sodium nitroprusside (0.3–3 ng ml −1 ) caused dose‐dependent relaxation of the rabbit mesenteric and coeliac arteries. 3 Iloprost (0.3–30 ng ml −1 ) and sodium nitroprusside (0.03–30 μg ml −1 ) caused dose‐dependent inhibition of rabbit platelet aggregation induced by adenosine diphosphate or collagen. 4 In combination, iloprost and sodium nitroprusside caused an inhibition of platelet aggregation that was 2–3 fold greater than would be expected by summation, while no such potentiation was observed on vascular smooth muscle. 5 Thus, our results indicate that under physiological conditions the mediators prostacyclin and endothelium‐derived relaxing factor (NO) can exert a synergistic action on platelets, but have only an additive effect on vascular smooth muscle.