Raised levels of plasma vascular endothelial growth factor (VEGF) are found
in some cancers, diabetes, and certain other conditions, but levels of its
receptor, soluble Flt-1 (sFlt-1), in these diseases have yet to be reporte
d. We hypothesised that smoking would influence levels of these molecules.
Consequently, we measured VEGF and sFlt-1 by enzyme-linked immunosorbent as
say (ELISA) in plasma from 92 non-smokers and 35 smokers. No difference in
VEGF was seen between the groups but, despite considerable overlap, sFlt-1
was significantly lower in smokers (P = 0.027). VEGF and sFlt-1 correlated
strongly with each other (P <0.001). Although VEGF may arise from a number
of cell types, including endothelial cells, the primary source of sFlt-1 is
thought to be the endothelium; however, neither VEGF nor sFlt-1 correlated
with levels of the endothelial cell activation/damage marker soluble throm
bomodulin. Our data point to changes in levels of the VEGF receptor, sFlt-1
- but not VEGF itself - in smokers, which appears to be unrelated to endot
helial cell function.