Pharmacological modification of bradykinin induced breakdown of the blood-brain barrier.
Internal carotid artery infusion of bradykinin caused extensive breakdown of the blood-brain barrier to protein as demonstrated by the extravasation of the marker, horseradish peroxidase, into vessel walls and the adjacent parenchyma. Pretreatment of the animals with indomethacin, trifluoperazine, or imidazole significantly reduced the quantity of abnormally permeable vessels as determined by light microscopy. By electron microscopy, it was determined that bradykinin caused an intense increase in the number of pinocytotic vesicles in the permeable segments, but no change in the interendothelial junctions. After imidazole pretreatment, although the extent of the permeability change was markedly reduced, the intensity of pinocytotic activity in the involved areas was not altered.
D000818:Animals; D001160:Arterioles / Q000648:ultrastructure; D001794:Blood Pressure / Q000187:drug effects; D001812:Blood-Brain Barrier / Q000187:drug effects*; D001920:Bradykinin / Q000494:pharmacology*; D002540:Cerebral Cortex / Q000098:blood supply / Q000648:ultrastructure; D005260:Female; D006735:Horseradish Peroxidase; D007093:Imidazoles / Q000494:pharmacology; D007213:Indomethacin / Q000494:pharmacology; D008854:Microscopy, Electron; D010873:Pinocytosis / Q000187:drug effects; D051381:Rats; D011919:Rats, Inbred Strains; D014268:Trifluoperazine / Q000494:pharmacology
D007093:Imidazoles; D014268:Trifluoperazine; C029899:imidazole; D006735:Horseradish Peroxidase; D001920:Bradykinin; D007213:Indomethacin