Epidemiological studies have shown an association between ambient levels of
particulate matter (PM) and increased mortality from cardiovascular diseas
es. However, the underlying mechanisms are still not clear. We hypothesised
that PM, when translocated after inhalation, could affect vascular smooth
muscle function. Therefore, total suspended particulate matter (TSP) was sa
mpled and investigated for its ability to affect aortic muscle contraction.
Both TSP and TSP supernatant (TSP-sup) induced a concentration-dependent r
elaxation of phenylephrine (PE)-precontracted aortic rings. Relaxation indu
ced by 300 mug/ml TSP was 51.5 +/- 3.1% of total contraction. At 60 and 100
mug/ml, relaxation induced by TSP was significantly higher compared to TSP
-sup. Ultrafine TiO2, used as a model to investigate the role of ultrafine
particles, did not show an effect. Soluble iron, present in TSP suspensions
, seems not to be involved, as chelating with deferoxamine did not affect T
SP-induced relaxation. However, TSP effects were inhibited by Trolox, sugge
sting a role of oxidants. Nudation of aortic rings showed that effects of T
SP were only partly endothelium-dependent, while preincubation with L-NAME
increased TSP-induced relaxation. From these data, we conclude that both th
e particle core and soluble components of TSP can affect the smooth muscle
function, leading to changes in the vascular contractile response.