The present review deals with the vascular action of calcium antagonists (CA) at the cellular level, emphasizing the interference between CA and postsynaptic alpha 2-adrenoceptors in the resistance vessels. 2. This interference, which can be demonstrated in various animal species, implicates that the pressor effect of an alpha 2-adrenoceptor agonist is diminished by the CA and by N alpha 2-EDTA. However, the vasoconstriction initiated by alpha 1-adrenoceptor agonists is hardly reduced by CA. Accordingly, the interaction is selective for alpha 2-adrenoceptors. 3. The following hypothesis is submitted: After formation of the alpha 2-adrenoceptor/agonist complex there occurs a transmembranous influx of extracellular calcium ions. This influx, which is inhibited by CA, is probably indispensable for the activation of contractile proteins. 4. Accordingly, the vasodilator activity of the CA might be explained as follows: the CA inhibit the alpha 2-receptor mediated component of the vasoconstriction, induced by endogenous catecholamines, without influencing the alpha 1-receptor component of the pressor effect.