Dog saphenous vein spiral strips were employed to determine whether an intracellular source of Ca2+ is used for contraction upon activation of the α2-adrenoceptor by B-HT 920 in Ca2+-free Krebs solution containing 50 μM EGTA. The studies were carried out in parallel with the activation of the α1-adrenoceptor by phenylephrine (Phe) under the condition that B-HT 920 (10−5 M) and Phe (2 × 10−6 M) gave rise to a similar level of responses in Ca2+-containing Krebs solution. A similar level of responses to these agonists at equieffective concentrations in Ca2+-free medium were also observed. Such responses to Phe and B-HT 920 were inhibited by 10−7 M rauwolscine and 10−7 M prazosin, respectively, and were not affected by 10−7 M nifedipine or 5 mM Mn2+. The responses to B-HT 920 (10−5 M) and submaximal concentration of Phe (2 × 10−6 M) in Ca2+-free medium were additive. However, if the vascular strips were first contracted maximally with 10−4 M Phe in Ca+2-free medium to deplete the intracellular Ca store, subsequent addition of B-HT 920 failed to induce additional response. Our results strongly suggest that activation of α2-adrenoceptor in dog saphenous vein in Ca2+-free medium indeed utilizes intracellular Ca2+ for contraction. We also found that the failure of earlier studies to demonstrate the contractile effects of B-HT 920 in dog saphenous vein was due to experimental artifacts derived from the use of high concentration of EGTA and artificial pH-buffering reagent.Key words: adrenoceptor, saphenous vein, vascular muscle, calcium.