Abstract: Smoking is one of the most important risk factors for cerebral circulatory disorders and nicotine is considered to be the major pathogenic compound in cigarette smoke. Amelioration of nicotine-induced vasoconstrictions (or vasodilations) may provide a therapeutic target for the treatment of stroke. This study will review the involvement of arachidonic acid metabolites pathway and nicotinic acetylcholine receptors (nAChRs) on nicotine-induced contractions (or relaxations) in the basilar artery. Arachidonic acid metabolites pathway and nAChRs may be new drug targets and their selectivity antagonists (or agonists) may be new therapeutic drugs for the treatment of stroke.