Using a perfusion technique of isolated vessels, vasoconstrictor responses to alpha-adrenoceptor agonists (norepinephrine [NE], phenylephrine [PE], clonidine, xylazine and tyramine) and KCl were investigated in isolated, perfused dog and monkey lingual arteries. A stainless steel cannula was inserted into the lingual artery segment and perfused with Krebs-Henseleit solution at a constant flow rate. In dog lingual arteries, the agonists induced vasoconstrictions with the following order of potency: NE > PE > tyramine >> clonidine > xylazine > KCl. In monkey preparations, the order was NE > PE >> clonidine greater-than-or-equal-to tyramine > xylazine > KCl. In both preparations, NE- and PE-induced constrictions were blocked by bunazosin (an alpha-1 adrenoceptor antagonist), but not influenced by midaglizole (a potent alpha-2 antagonist). Diltiazem (a Ca entry blocker) significantly attenuated NE-induced vasoconstrictions in dog lingual arteries, but did not significantly influence these in monkey preparations. These results suggest that: [1] these arteries contain mostly alpha-1 but scarcely any alpha-2 adrenoceptors; [2] in dog preparations, tyramine induced a marked vasoconstriction which may contribute to investigation on the mechanisms of catecholamine releases from sympathetic nerve terminals; and [3] different blocking effects of diltiazem may indicate that extracellular Ca++ influx may have varying degrees of importance in alpha-1 adrenoreceptor-mediated constrictions in different species, although participation of an intracellular mechanism might not be ruled out.