A fibrin(ogen) derived pentapeptide induces vasodilation, prostacyclin release and an increase in cyclic AMP.
A pentapeptide derived from fibrin(ogen), Ala-Arg-Pro-Ala-Lys, is known to increase microvascular permeability. This peptide induced dilation of bovine mesenteric arteries and caused a release of prostacyclin and an increase in cyclic AMP in these vessels. These changes were abolished by pretreatment with indomethacin, indicating that the vasodilation and the increase in cyclic AMP are due to the prostacyclin release. One mechanism underlying the effect of this peptide on microvascular permeability might thus be a triggering of the arachidonic acid cascade, with release of prostacyclin and an increased blood flow, which may potentiate the effect of other substances with a direct effect on vascular endothelium, e.g. histamine. The pentapeptide is known to release histamine from mast cells.
D000818:Animals; D002417:Cattle; D000242:Cyclic AMP / Q000097:blood*; D011464:Epoprostenol / Q000378:metabolism*; D005338:Fibrin Fibrinogen Degradation Products / Q000494:pharmacology*; D066298:In Vitro Techniques; D009842:Oligopeptides / Q000494:pharmacology*; D011453:Prostaglandins / Q000378:metabolism*; D014664:Vasodilation / Q000187:drug effects*
D005338:Fibrin Fibrinogen Degradation Products; D009842:Oligopeptides; D011453:Prostaglandins; D011464:Epoprostenol; D000242:Cyclic AMP