Thromb Haemost 1994; 72(02): 318-321
DOI: 10.1055/s-0038-1648860
Original Article
Schattauer GmbH Stuttgart

Desulfated Hirugen (Hirudin 54-65) Induces Endothelium-Dependent Relaxation of Porcine Pulmonary Arteries

Erika Glusa
The University of Jena, Medical School, Center for Vascular Biology and Medicine, Erfurt, Germany
› Author Affiliations
Further Information

Publication History

Received 03 February 1994

Accepted after revision 13 April 1994

Publication Date:
24 July 2018 (online)

Summary

Desulfated hirugen (hirudin 54-65) at concentrations from 0.1 to 2 μM was found to relax PGF-precontracted ring segments of porcine pulmonary arteries with intact endothelium. The relaxation was associated with a pronounced increase in cGMP in the vessels. This endothelium-dependent relaxant effect depended on the extracellular calcium ion concentration and was probably due to the release of endothelium-derived NO as indicated by its susceptibility to blockade of the NO synthesis by NG-nitro-L-arginine. In the presence of indomethacin (3 μM) the maximum hirugen effect was significantly diminished by about 25%. In contrast, neither the sulfated hirugen nor recombinant desulfato hirudin at equimolar concentrations exerted endothelium-dependent relaxation. Hence, the relaxant effect did not correspond to the anticoagulant activity. Desulfated hirugen can be assigned to the group of well-known peptides causing vasodilatation via an endothelium-dependent mechanism.

 
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