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• W2022089615 abstract "We hypothesized that endotoxin (LPS) would impair bradykinin (BK)-induced calcium (Ca2+) mobilization in aortic endothelial cells, perhaps due to cytotoxicity or via stimulation of nitric oxide (NO) synthesis. As well, we sought to define contributions of LPS-stimulated Ca2+ mobilization to these effects.LPS- or BK-induced increments of intracellular Ca2+ were assessed by microspectrofluorimetry with fura-2 in passaged bovine aortic endothelial cells. Time- and dose-dependent effects of LPS exposure (+/- inhibitors of NO or prostaglandin synthesis) on subsequent BK-induced Ca2+ mobilization and on attached cell counts were determined.LPS (0.1 to 1.0 mg/ml) led to rapid increments of Ca2+, while Ca2+ responses were delayed following LPS (1 to 10 microg/ml) and lower doses were without effect. By contrast, LPS more potently (1.0 pg to 1.0 microg/ml) led to dose- and time-dependent impairment of subsequent BK-induced Ca2+ mobilization, with peak effect at four to six hours, persisting for at least 18 hours. This delayed effect on BK-response was unaltered by inhibition of either NO synthase or cyclooxygenase. The effect of LPS on BK-responsivity depended importantly on cell confluence, as it was not observed in subconfluent cells. By contrast, LPS-induced cell detachment, which was observed only at doses > or = 1.0 microg/ml, did not depend on confluence.Different mechanisms lead to endothelial cytotoxicity and to impaired BK-response following LPS. Only the former effect, occurring at higher doses, might depend on initial LPS-induced Ca2+ mobilization." @default.
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• W2022089615 date "1998-10-01" @default.
• W2022089615 modified "2023-09-26" @default.
• W2022089615 title "Selectivity of endotoxin-induced defect in endothelial calcium mobilization" @default.
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• W2022089615 doi "https://doi.org/10.1046/j.1523-1755.1998.00090.x" @default.
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