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Thromb Haemost 1996; 76(03): 469-474
DOI: 10.1055/s-0038-1650601
Original Article
Schattauer GmbH Stuttgart

Inhibitory Effect of Prostacyclin and Nitroprusside on Type IIB von Willebrand Factor-promoted Platelet Activation

Mariangela Francesconi
The Department of Biological Chemistry and Unit for the Study of Biomembranes of C.N.R, Italy
,
Alessandra Casonato
1   The institute of Medical Semeiotics and Fourth Chair of Internal Medicine, University of Padova, Italy
,
Stefano Pagan
The Department of Biological Chemistry and Unit for the Study of Biomembranes of C.N.R, Italy
,
Arianna Donella-Deana
The Department of Biological Chemistry and Unit for the Study of Biomembranes of C.N.R, Italy
,
Elena Pontara
1   The institute of Medical Semeiotics and Fourth Chair of Internal Medicine, University of Padova, Italy
,
Antonio Girolami
1   The institute of Medical Semeiotics and Fourth Chair of Internal Medicine, University of Padova, Italy
,
Renzo Deana
The Department of Biological Chemistry and Unit for the Study of Biomembranes of C.N.R, Italy
› Author Affiliations
Further Information

Publication History

Received 17 August 1995

Accepted after resubmission 29 May 1996

Publication Date:
10 July 2018 (online)

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Summary

Von Willebrand disease (vWD) of type IIB is a hereditary haemorragic 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.

The present report shows that prostacyclin and nitroprusside, vaso-dilator-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. Type IIB vWF also elicits tyrosine phosphorylation of proteins with apparent molecular mass of 60,74,82 and 130 kDa. Prostacyclin, which induces per se tyrosine-phosphoryla-tion of proteins of about 38 and 45 kDa, inhibits drastically the type IIB vWF-promoted tyrosine-phosphorylation of the 74 kDa protein while inhibits slightly that of 60 kDa band. The protein tyrosine-kinase inhibitor genistein causes a little decrease in the type IIB vWF-induced release of arachidonic acid.

It is concluded that the inhibition exerted by prostacyclin and nitroprusside on type IIB vWF-elicited platelet activation seems to be largely ascribable to prevention of the phospholipase A2 activation with the ensuing decrease of the subsequent protein tyrosine phosphorylation

 

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