Abstract: Objective To study the mechanism underlying changes of vasoconstriction and vasodilatation functions in thoracic aorta of cigarette smoking rats. Methods A rat smoking model was established.Effects of no smoking,short-term,mid-term,and long-term heavy smoking on reactions of peeled rat thoracic aorta endothelium induced by KCl,phenylephrine（PE）,sodium nitroprusside（SNP）,tetraethyla-mmonium（TEA） and 4-aminopyridine（4-AP） were detected with in vitro vascular ring perfusion techniques. Results The contracting reactions of thoracic aorta to KCI and PE at the maximal concentration were（2.52±0.10）g and（2.60±0.08）g,（2.12±0.11）g and（2.21±0.11）g,respectively,in mid-term and long-term smoking groups,which were higher than those in control group（1.97±0.11）g and（1.61±0.10g）,（P＜0.05）.The dilating reaction rates of SNP at the maximal concentration were significantly lower in mid-term and long-term smoking groups than in control group（64.37%±5.12% and 61.27%±3.45% vs 91.16%±3.76%,P＜0.05）.The relative contracting reactions of thoracic aorta to TEA and 4-AP were（0.44±0.06）g and（0.40±0.07）g,（0.65±0.11）g and（0.60±0.09）g in mid-term and long-term smoking groups,which were significantly lower than those in control group（0.68±0.10）g and（1.02±0.15）g,P＜0.05.The reaction intensity was positively related with the smoking time. Conclusion Cigarette smoking can increase the contracting function and decrease the dilating function of arteries.TEA and 4-AP can reduce the contracting reaction of thoracic aorta.Change in arterial function may be related to the function of K channels.