Epidemiological evidence shows that air pollutant levels positively correlate with increases in both acute and chronic cardiovascular disease. The pollutant diesel exhaust (DE) increases endothelin (ET) levels, suggesting this may contribute to DE-induced cardiovascular disease. We hypothesized that acute exposure to DE also enhances ET-1-meditated coronary artery constrictor sensitivity. Constrictor responses to KCl, U46619, and ET-1 were recorded in pressurized intraseptal coronary arteries from rats exposed for 5 h to DE (300 µg/m³) or air using a video microscopy system. ET-1 constrictor responses were augmented in arteries from DE-exposed rats. Nitric oxide synthase (NOS) inhibition (N-nitro-L-arginine, L-NNA, 100µM) or inactivation of the endothelium augmented ET-1 responses in arteries from AIR but not DE rats so that after either treatment, responses between groups were not different. DE exposure did not affect KCl and U46619 constrictor responses but NOS inhibition equally augmented KCl constriction in both groups, suggesting basal NOS activity is not affected by DE exposure. The ET_B receptor antagonist BQ-788 (10 µM) inhibited ET-1 constriction only in DE-exposed arteries and constriction in the presence of the antagonist was not different between groups. In summary, a 5-h DE exposure selectively increases constrictor sensitivity to ET-1. This augmentation is endothelium- and ET_B receptor-dependent. These data suggest DE exposure diminishes ET_B receptor activation of endothelial NOS and augments ET_B-dependent vasoconstriction. This augmented coronary vasoreactivity to ET-1 following DE, coupled with previous reports that DE-induces production of ET-1, suggests that ET-1 may contribute to the increased incidence of cardiac events during acute increases in air pollution levels.