Arteries were isolated from male DBA/2 mice and mounted on a small vessel wire myograph for isometric recording. Responses to exogenous noradrenaline were inhibited with high affinity by prazosin (pKB, 9.3) and 5-methyl-urapidil (pKB, 9.2) and with low affinity by 8-[2-[4-(2-methoxyphenyl)-1 piperazinyl]ethyl]-8-azaspiro[4.5]decane-7,9-dione (BMY 7378) (pA(2), 6.7). Chloroethylclonidine (10 microM) produced only a small reduction in the maximum response to noradrenaline. Responses to electrical field stimulation were also inhibited with high affinity by prazosin (pIC50, 9.3-9.5) and 5-methyl-urapidil (pIC50, 8.0-8.3). Responses were sensitive to BMY 7378 at low frequencies of stimulation (pIC50 at 2 Hz, 8.2) but not at high frequencies (pIC50 at 20 Hz, 6.5). In conclusion, contractions to exogenous and endogenous noradrenaline in mouse femoral small arteries are mediated mainly by alpha1A-adrenoceptors. alpha1D-adrenoceptors are not involved in responses to exogenous noradrenaline but appear to be activated by neurally released noradrenaline at a low frequency of stimulation.