Journal of Applied Physiology, Vol 50, Issue 6 1212-1219, Copyright © 1981 by American Physiological Society
Depression of serotonin uptake by cultured endothelial cells exposed to high O2 tension
E. R. Block and S. A. Stalcup
Serotonin (5-hydroxytryptamine, 5-HT), a vasoactive amine, is removed from
the pulmonary circulation by active transcellular transport into
endothelial cells, followed by intracellular metabolism. Pulmonary uptake
of 5-HT is depressed by high partial pressures of O2 (Po2). To
characterized the cellular basis and mechanism for hyperoxic depression of
lung 5-HT uptake, we evaluated the effect of high Po2 on 5-HT uptake by
calf aortic endothelial cells in primary confluent monolayer. Cells were
exposed to either 95% O2, or 14% O2 (controls) in 5% Co2 at 1 ATA for 20 or
42 h. Following exposure 5-[14C]HT (1 X 10-7 M) was added to the culture
medium, and 5-HT uptake in pmol/10(6) cells was measured. Exposure to 95%
O2 for 20 h or 42 H resulted in significant depression of 5-HT uptake by
cultured endothelial cells, and uptakes remained significantly depressed 48
h after exposure to 95% O2 had ended. Inhibition of intracellular
metabolism of 5-HT by iproniazid did not affect 5-HT uptake by control or
O2-exposed endothelial cells. These results indicate that 1) high Po2
levels depress 5-HT uptake in endothelial cells by direct inhibition of the
transcellular transport of 5-HT and 2) hyperoxic depression of 5-HT uptake
in cultured endothelial cells is not readily reversible.
