Application | Comment | Organism |
---|---|---|
medicine | plasmin induces an endothelium-dependent NO-mediated vasorelaxation in the porcine coronary artery, whereas it inhibits the endothelium-dependent relaxation induced by thrombin | Sus scrofa |
Inhibitors | Comment | Organism | Structure |
---|---|---|---|
4-amidinophenyl methane-sulfonyl fluoride | abolishes plasmin-induced Ca2+ elevation by its pretreatment of plasmin | Homo sapiens | |
4-amidinophenyl methane-sulfonyl fluoride | substantially abrogates the relaxing effect of plasmin. Abolishes plasmin-induced Ca2+ elevation by its pretreatment of plasmin | Sus scrofa | |
additional information | pretreatment with plasmin, thrombin and trypsin significantly but, only partly, attenuates subsequent relaxation induced by plasmin. Major part of the plasmin-induced relaxation is resistant to these pretreatments | Sus scrofa | |
Nomega-nitro-L-arginine methyl ester | almost completely abolishes plasmin-induced relaxation | Sus scrofa | |
Tranexamic acid | substantially abrogates the relaxing effect of plasmin | Sus scrofa |
Organism | UniProt | Comment | Textmining |
---|---|---|---|
Homo sapiens | - |
- |
- |
Sus scrofa | - |
- |
- |
Source Tissue | Comment | Organism | Textmining |
---|---|---|---|
HUVEC cell | plasmin induces a concentration-dependent transient elevation in the cytosolic Ca2+ concentrations | Homo sapiens | - |
additional information | in PCAEC cells, plasmin induces an endothelium-dependent relaxation and a concentration-dependent transient elevation in the cytosolic Ca2+ concentrations. Plasmin concentration-dependently induces NO production | Sus scrofa | - |