By the extracellular recording technique, the action potentials and spontaneous contractions of the isolated rat longitudinal portal vein strips were simultaneously recorded in the presence of varying concentrations of electrolytes, various vasoactive agents, and hormones, and the mechanisms regulating the force and frequency of spontaneous contraction of the vascular smooth muscle were investigated. A longitudinal stretch (-200% of the initial length), a higher [K+]0 (-30 mM), a lower [Na+]0, epinephrine, acetylcholine or ouabain increased both force and frequency of the phasic contractions. A lower [Na+]0 or ouabain raised basal tone of the muscle in addition to the above effects. A higher [Ca++]0 increased the contractile force, while it decreased the frequency. A lower [Ca++]0, calcium channel blocker or VIP reduced the contractile force but increased the contractile frequency. A bigger force and a higher frequency of the phasic contractions were exhibited in the portal vein strips isolated from rats with CCl4-induced experimental portal vein hypertension. They were similar to responses of the strips from the intact rats to stretch, ouabain, or higher [Ca++]0 in the presence of lower [Na+]0. These results suggest that an initiation and force of the phasic and tonic contractions depend on extracellular Ca++ concentration and influx of Ca++, and frequency of the phasic contractions, mainly on membrane potential rather than on extracellular Ca++ concentration. In the portal hypertension, permeability of the cell membrane to Ca++ is possibly increased.