Lysophosphatidylcholine alters vascular tone in rat aorta by suppressing endothelial [Ca2+]i signaling

The detailed mechanism of how lysophosphatidylcholine (LPC) suppresses endothelium-dependent vasodilatation is unclear at present. We investigated the effects of LPC on endothelial intracellular calcium (EC [Ca2+](i)) Signaling and vascular tone simultaneously using a new technique we developed. Fura-2-labeled rat aortic specimens were mounted in a tissue flow chamber and precontracted with phenylephrine (5 x 10(-8) M). Under either basal or agonist-stimulated conditions, the EC [Ca2+](i), level was calculated from fura 2 fluorescence ratio images, and the vasculartone was estimated by measuring the relative displacement of the fluorescence images. Although both acetylcholine (ACh)-induced EC [Ca2+], elevation and the concomitant vasorelaxation were partially suppressed in specimens pretreated with LPC (20 muM), the quantitative relationship between EC [Ca2+], elevation and the corresponding vasorelaxation was unaffected. A high concentration of LPC (40 muM) completely eliminated ACh-evoked [Ca2+](i) elevation and vasodilatation. It has been reported that exposing vascular tissue to a calcium-free buffer causes a reduction in the EC [Ca2+](i) level and the accompanying vasoconstriction. Pretreatment with 20 muM LPC reduced the basal EC [Ca2+](i), level and abolished the calcium-free solution-induced EC [Ca2+](i) reduction and vasoconstriction. We conclude that LPC impairs endothelium-dependent vasorelaxation mainly by reducing the basal EC [Ca2+](i) level and suppressing agonist-evoked EC [Ca2+](i) signaling. Copyright (C) 2002 National Science Council, ROC and S. Karger AG, Basel.