Experiments were conducted to determine whether Sprague-Dawley rats from different suppliers have the same hypertensive response to chronic inhibition of nitric oxide synthase. Rats (240-260 g) obtained from either Harlan or Charles River Laboratories were maintained in metabolic cages for baseline (week 0) measurements before receiving Nω-nitro-L-arginine methyl ester (L- NAME) in the drinking water for 2 wk at 5 or 65 mg · kg-1 · day-1. Baseline values for tail cuff pressure (TCP) were significantly higher in Harlan rats (131 ± 2 mmHg) compared with Charles River rats (108 ± 3 mmHg, P < 0.001). At 65 mg · kg-1 · day-1, L-NAME produced a significantly larger increase in TCP in Harlan versus Charles River rats (41 ± 4 vs. 29 ± 4%, respectively, P < 0.01). Food and water intake and sodium and water excretion were not different between groups. Urinary excretion of nitrate and nitrite (U(NO(x)) V) was significantly reduced in all rats given L-NAME, U(NO(x)) V(x) was decreased by 69 ± 12 and 62 ± 7% in Harlan and Charles River rats, respectively. The lower dose of L-NAME increased TCP and decreased U(NO(x)) V in both Harlan and Charles River rats; these effects were more pronounced in the Harlan rats. These results suggest that NO plays a more significant role in the maintenance of arterial pressure in Sprague- Dawley rats from Harlan compared with Charles River Laboratories. Such findings may also provide insight as to why some of the mechanisms associated with chronic L-NAME treatment are not consistent between laboratories.