We examined whether alpha 1-adrenoceptor-mediated vasoconstrictions were due to extra- or intracellular Ca2+ movements, and whether they were subdivided into alpha 1-adrenoceptor subtypes in dog and monkey lingual arteries. The NE-induced vasoconstriction in dog lingual arteries was mostly dependent on Ca2+ influx from the extracellular space, since it was readily blocked by a Ca2+ entry blocker, diltiazem, and the NE-induced response was attenuated approximately 90% in Ca(2+)-free solution. On the other hand, in monkey lingual arteries, diltiazem failed to depress the NE-induced dose-response curve, and the response was attenuated only about 60% in Ca(2+)-free solution. The vasoconstrictor response to 10mg caffeine in normal KHS was almost the same as that to 1 micrograms NE in Ca(2+)-free solution in both kinds of arteries, suggesting that alpha 1-adrenoceptor-mediating vasoconstrictions require a different number of sources of Ca2+ in different blood vessels. Pretreatment of preparations with CEC (an alpha 1B-antagonist) significantly suppressed and shifted the dose-response curve for NE to the right in monkey lingual arteries, but it had no significant effect in dog lingual arteries. However, WB4101 (an alpha 1A-antagonist) showed almost the same potency in blocking vasoconstrictor responses as bunazosin in both kinds of arteries (the pA2 values were not significantly different). Moreover, responses to ME (an alpha 1A-agonist) were blocked by diltiazem as well as by bunazosin and WB4101, while CEC had no blocking effect on ME-induced responses.(ABSTRACT TRUNCATED AT 250 WORDS)