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A fibrin(ogen) derived pentapeptide induces vasodilation, prostacyclin release and an increase in cyclic AMP
Abstract:
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.
Insights
A fibrin-derived pentapeptide increases microvascular permeability by triggering prostacyclin release, leading to vasodilation. This mechanism involves the arachidonic acid cascade and histamine release from mast cells.
Area of Science:
- Biochemistry
- Physiology
- Pharmacology
Background:
- A pentapeptide from fibrin(ogen), Ala-Arg-Pro-Ala-Lys, is recognized for its ability to enhance microvascular permeability.
- This peptide has been observed to induce vasodilation in bovine mesenteric arteries.
Purpose of the Study:
- To elucidate the mechanism by which the pentapeptide increases microvascular permeability.
- To investigate the role of prostacyclin and histamine release in the peptide's vascular effects.
Main Methods:
- Administration of the pentapeptide to bovine mesenteric arteries.
- Measurement of vascular permeability, vasodilation, prostacyclin release, cyclic AMP levels, and histamine release.
- Use of indomethacin to block prostaglandin synthesis.
Main Results:
- The pentapeptide induced vasodilation and increased cyclic AMP levels in mesenteric arteries.
- These effects were abolished by indomethacin, confirming prostacyclin release as the mediator.
- The pentapeptide was also found to trigger histamine release from mast cells.
Conclusions:
- The pentapeptide's effect on microvascular permeability is mediated by the release of prostacyclin via the arachidonic acid cascade.
- Histamine release from mast cells may also contribute to the peptide's vascular effects.
- This peptide offers a potential pathway to modulate vascular function and blood flow.