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Chronic smoking is associated with acetylcholine-dependent endothelial dysfunction, an early marker of atherosclerosis. The purpose of this study was to determine whether this effect of smoke exposure on blood vessel endothelium is reversible. New Zealand White rabbits were placed in a 240 cubic-foot air flow chamber for 3 hours per day, 5 days per week, over a 4-week period and were exposed to smoke produced by a robotic smoke generator. After the 4-week period, rabbits (n=four, Smoked) were killed and their superficial femoral arteries (SFAs) were cut into 3-mm segments. The rings were suspended from tension transducers and the maximal contraction of one ring was recorded following stimulation with norepinephrine (NE). The remaining rings were contracted to 50% of the maximum. Relaxation of these rings was determined by adding increasing doses of acetylcholine. The remaining rabbits were placed in and out of the chamber without smoke exposure for an additional 4 weeks (n=five, Reverse-smoked), and then the SFAs were harvested. Control (n=six) SFAs were explanted from rabbits not (continued on next page) (Abstract continued) exposed to smoke. KCl induced increased contractility in the smoked group when compared with the controls, and NE induced increased contractility in the smoked group when compared with the reverse-smoked rabbits. Acetylcholine-dependent relaxation was significantly reduced in the rings from the smoked rabbits when compared with the controls. The percentage ring relaxation in the reverse-smoked rabbits was similar to the control rings.The impaired acetylcholine-dependent endothelium relaxation in the smoked group verifies endothelial injury. However, the improved relaxation in the reverse-smoked group suggests that endothelial injury is reversible.