Release of prostacyclin from cultured human endothelial cells following prolonged exposure to histamine.
Histamine is an important pro-inflammatory molecule mediating leukocyte margination, plasma extravasation and vasodilation, but its precise mode of action on vascular endothelium is unclear. We report that histamine is able to induce prolonged release of prostacyclin (PGI2) from human endothelial cells via occupancy of the H1 receptor, without an absolute requirement for the presence of histamine or synthesis of new enzyme protein to facilitate continued release of PGI2.
Bull
H A
HA
Department of Dermatology, Middlesex Hospital, London, U.K.
Rustin
M H
MH
Dowd
P M
PM
D015056:1-Methyl-3-isobutylxanthine / Q000494:pharmacology; D000900:Anti-Bacterial Agents / Q000494:pharmacology; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology; D003994:Bucladesine / Q000494:pharmacology; D002478:Cells, Cultured; D004730:Endothelium, Vascular / Q000187:drug effects* / Q000378:metabolism; D011464:Epoprostenol / Q000378:metabolism*; D006632:Histamine / Q000494:pharmacology*; D006633:Histamine Antagonists / Q000494:pharmacology; D006801:Humans; D014268:Trifluoperazine / Q000494:pharmacology
D000900:Anti-Bacterial Agents; D000894:Anti-Inflammatory Agents, Non-Steroidal; D006633:Histamine Antagonists; D014268:Trifluoperazine; D003994:Bucladesine; D006632:Histamine; D011464:Epoprostenol; D015056:1-Methyl-3-isobutylxanthine