This study aimed to investigate the mechanisms involved in the contractile effects produced by the novel quinoline derivative, 2-(2-aminoethyl)-quinoline (D-1997), in the canine isolated basilar artery. For comparison, the effects of D-1997 were also evaluated on rat aorta. Canine basilar artery and rat aortic rings were prepared and mounted in organ baths to record isometric tension changes. The contractile effects of D-1997 in the basilar artery were compared with those produced by 5-hydroxytryptamine (5-HT) and the 5-HT receptor agonist quipazine. Thus, 4-HT (10(-10)-10(-6)M), D-1997 (3.1 x 10(-8)-10(-4) M) and quipazine (3.1 x 10(-7)-10(-4) M) each caused concentration-dependent contractions of the canine basilar artery with a rank order of agonist potency of 5-HT > D-1997 > quipazine. 5-HT and D-1997 exhibited similar maximum effects which were higher than that of quipazine. Similar concentrations of D-1997 failed to produce contraction in rat aorta. The effects of D-1997 in the basilar artery were not modified by incubation with either the 5-HT2 receptor antagonist ketanserin (0.01-1 microM), the 5-HT3 and 5-HT4 receptor antagonist ICS205930 (tropisetron; 0.1-10 microM), the 5-HT1A receptor antagonist spiroxatrine (0.01-1 microM), the beta-adrenoceptor blocker with high affinity for 5-HT1A and 5-HT1B binding sites (+/-)-pindolol (0.01-1 microM), or the alpha 1-adrenoceptor antagonist prazosin (0.01-1 microM). In contrast, the D-1997-induced responses were potently and concentration-dependently antagonized by the mixed 5-HT1-like and 5-HT2 receptor antagonist methiothepin (0.01-1 microM). It is concluded that D-1997 contracts the canine basilar artery by stimulating 5-HT1-like receptors unrelated to either the 5-HT1A or 5-HT1B receptor subtypes. The compound seems to be devoid of 5-HT2 receptor agonist properties in rat aorta.