Current literature suggests that chronic nitric oxide synthase (NOS) inhibition has differential effects on endothelium-dependent dilation (EDD) of conduit arteries versus arterioles. Therefore, we hypothesized that chronic inhibition of NOS would impair EDD of porcine left anterior descending (LAD) coronary arteries but not coronary arterioles. Thirty-nine female Yucatan miniature swine were included in the study. Animals drank either tap water or water with NG-nitro-L-arginine methyl ester (L-NAME, 100 mg/L), resulting in Control and Chronic NOS Inhibition (CNI) groups, respectively. Treatment was continued for 1-3 months (8.3±0.6 mg/kg/day). In vitro EDD of coronary LADs and arterioles was assessed via responses to adenosine diphosphate (ADP, LADs only) and bradykinin (BK), and endothelium-independent function was assessed via responses to sodium nitroprusside (SNP). Chronic NOS inhibition diminished coronary artery EDD to ADP and BK. Incubating LAD rings with L-NAME decreased relaxation responses of LADs from Control pigs, but not CNI pigs, such that between-group differences were abolished. Neither indomethacin (Indo) nor sulfaphenazole incubation significantly affected relaxation responses of LAD rings to ADP or BK. Coronary arteries from CNI pigs showed enhanced relaxation responses to SNP. In contrast to coronary arteries, coronary arterioles from CNI pigs demonstrated preserved EDD to BK and no increase in dilation responses to SNP. Neither L-NAME, Indo, nor L-NAME+Indo incubation resulted in significant between-group differences in arteriole dilation responses to BK. These results suggest that while chronic NOS inhibition diminishes EDD of LAD rings, most likely via a NOS-dependent mechanism, it does not affect EDD of coronary arterioles.