Title : Inhibitory effect of prostacyclin and nitroprusside on type IIB von Willebrand factor-promoted platelet activation.

Pub. Date : 1996 Sep

PMID : 8883288






4 Functional Relationships(s)
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1 Von Willebrand disease (vWD) of type IIB is a hereditary haemorrhagic disorder characterised by an excessive interaction of von Willebrand factor (vWF) with the platelet receptor GPIb which promotes platelet activation and aggregation through a phospholipase A2-mediated release of arachidonic acid. Arachidonic Acid von Willebrand factor Homo sapiens
2 Von Willebrand disease (vWD) of type IIB is a hereditary haemorrhagic disorder characterised by an excessive interaction of von Willebrand factor (vWF) with the platelet receptor GPIb which promotes platelet activation and aggregation through a phospholipase A2-mediated release of arachidonic acid. Arachidonic Acid von Willebrand factor Homo sapiens
3 The present report shows that prostacyclin and nitroprusside, vasodilator-compounds that enhance the cAMP and cGMP concentration respectively, cause a drastic inhibition of the type IIB vWF-induced platelet responses including increase of cytosolic Ca2+ concentration, phosphorylation of pleckstrin (47 kDa) and myosin light chain (20 kDa), secretion of ATP and serotonin, and aggregation parallel to a decrease of arachidonic acid release. Arachidonic Acid von Willebrand factor Homo sapiens
4 The protein tyrosine-kinase inhibitor genistein causes a little decrease in the type IIB vWF-induced release of arachidonic acid. Arachidonic Acid von Willebrand factor Homo sapiens