PMID: 1996698Feb 1, 1991Paper

Oxidative stress inhibits bradykinin-stimulated 45Ca2+ flux in pulmonary vascular endothelial cells

The American Journal of Physiology
S J Elliott, W P Schilling


The effects of oxidant stress and altered glutathione reductase activity on agonist-induced flux of Ca2+ were studied in cultured calf pulmonary artery endothelial cells using radioisotopic 45Ca2+. Bradykinin-stimulated uptake of 45Ca2+ was determined after cells were incubated with the membrane-permeant oxidant t-butylhydroperoxide (0.4 mM) for various durations. t-Butylhydroperoxide increased uptake of 45Ca2+ under basal conditions and significantly decreased bradykinin-stimulated uptake in a time-dependent manner through incubation periods of 2 h. Preincubation of cells with 1,3-bis(chloroethyl)-1-nitrosourea markedly reduced bradykinin-stimulated uptake in cells subsequently treated with t-butylhydroperoxide. Bradykinin-stimulated efflux of 45Ca2+ and 86Rb+ was examined in control and oxidant-stressed endothelial cells. t-Butylhydroperoxide initially decreased bradykinin-stimulated efflux of 45Ca2+ but had no effect on 86Rb+ efflux. After more prolonged incubation with the oxidant, stimulated 45Ca2+ efflux was further inhibited, and basal efflux of 86Rb+ was increased to a rate similar to that observed with bradykinin stimulation. Elevated basal 86Rb+ efflux was blocked by tetrabutylammonium chloride, a selective inhibitor ...Continue Reading

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