Article révisé par les pairs
Résumé : BACKGROUND:: Epidemiological and clinical studies have shown that traffic-related air pollution and, particularly, diesel exhaust particles (DEP) are strongly linked to cardiovascular mortality. METHODS:: Vascular toxicity was studied by assessing vasomotor responses of aortas isolated from normotensive Wistar rats exposed in vitro to DEP (DEP suspension and aqueous DEP extract). In vivo experiments were performed on Wistar rats and spontaneously hypertensive rats (SHR) exposed for 4 weeks via intratracheal instillation to either DEP or saline vehicle. After sacrifice, vascular responses to acetylcholine (ACh) or sodium nitroprusside (SNP) were assessed in vitro and the expression of p22phox, a major NADPH oxidase subunit, was studied by RTq-PCR. RESULTS:: In aortas from Wistar rats, in vitro DEP incubation (both preparations) markedly inhibited the relaxations to ACh and slightly to SNP; this effect was reversed in the presence of superoxide dismutase. In contrast, in aortas from in vivo-exposed animals, ACh-induced relaxations were only significantly impaired in the SHR group, accompanied with a significant up-regulation of p22phox, and no change in systolic blood pressure. CONCLUSIONS:: Although in vitro exposure to DEP produces a vascular oxidative stress, repeated in vivo exposures to DEP only impair vascular function in SHR, via an up-regulation of p22phox. This suggests a synergistic effect on endothelial dysfunction between particulate air pollution and hypertension.

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