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• W2324376012 abstract "The involvement of histamine-receptor subtypes in histamine-induced release of nitric oxide (NO) from porcine aortic endothelial cells was studied. NO release was measured directly by using an NO electrode and by electron paramagnetic resonance (EPR) spin trapping. NO release induced by histamine (200 μM) was reduced in the presence of 2 μM cimetidine, an H2-receptor antagonist, but not altered by 2 μM pyrilamine, an H1-receptor antagonist. Histamine-induced NO release was significantly reduced by the addition of 20 μM of the Rp diastereomer of adenosine cyclic 3′,5′-phosphorothioate (Rp-cAMPS), a membrane-permeable antagonist of cyclic adenosine monophosphate (cAMP). Application of 100 μM forskolin, an activator of adenylate cyclase, induced NO release from porcine aortic endothelial cells. Fura-2 acetoxymethylester (fura-2/AM) studies showed that addition of 100 μM histamine did not produce any significant increase in the use of free concentration of intracellular Ca2+. These results suggest that in porcine aortic endothelial cells, NO-mediated vasodilation might be caused by production of cAMP initiated through the histamine H2-receptor." @default.
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• W2324376012 date "1998-08-01" @default.
• W2324376012 modified "2023-10-18" @default.
• W2324376012 title "Histamine H2-Receptor-Mediated Nitric Oxide Release from Porcine Endothelial Cells" @default.
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• W2324376012 doi "https://doi.org/10.1097/00005344-199808000-00002" @default.
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