The effects of ajmaline on vascular smooth muscle were studied using helical aortic strips and portal veins of male rats. This report is based on the results of 104 mechanical experiments. In 30 additional experiments electrical activity was recorded simultaneously at different points of the preparation using extracellular methods (liquid paraffine or pressure electrodes technique). Ajmaline induces relaxation of aortic helical strips (activated by 2.0 µg/l norepinephrine) to 75% of initial tension in a dose of 0.6 mg/l, to 50% by 2.0 mg/l, and to 25% by 4–5 mg/l. The relaxation slope is shifted to the right by increasing the [Ca<sup>++</sup>]<sub>o</sub> from 2.0 to 4.0 mM, by increasing the initial norepinephrine concentration to 4.0–10 µg/l, or by KC1 depolarization, [K<sup>+</sup>]<sub>o</sub> ranging from 15 to 60 mM.The relaxing effect of ajmaline on aortic strips can partly be attributed to a change in electrical activity with a dose-dependent conduction impairment or block and, at high concentrations, also a decrease in the frequency of pacemaker excitations. Experiments on aortic strips in K<sup>+</sup> contracture show relaxation independent of changes in phasic electrical events. Ajmaline ranging from 0.2 to 80–100 mg/l causes on the portal vein a marked increase in amplitude and a small decrease in frequency of rhythmical contractions. Integrated isometric force reaches 300% of initial values. The increasing amplitude of contractions is related to a prolongation of excitation trains, while the frequency and amplitude of the individual spike are reduced.Our results suggest that the effects of ajmaline on the mechanical and electrical activity of vascular smooth muscle may be partly related to a reduction in Ca<sup>++</sup> and probably Na<sup>+</sup> conductance.