Aequorin was loaded into cells of the ferret portal vein in order to follow intracellular Ca2+ levels during smooth muscle contraction. In response to a single d.c. pulse, the aequorin signal reaches a peak during the rising phase of the evoked force transient and begins to rapidly fall while force is still rising. In response to the addition of phenylephrine to the bathing solution, the aequorin signal rises rapidly to a peak while force is still rising but then falls rapidly to a lower level from which it declines more slowly, staying above base-line levels as long as force is maintained. In response to the elevation of K+ concentration in the bathing solution, light and force rise together and the elevated light level is maintained as long as is force. With increasing concentrations of K+, force increases up to a concentration of 50-60 mM but light increases up to 90 mM, suggesting that at a concentration of 50-60 mM-K+, the Ca2+ concentration may be saturating with respect to a site of action on the contractile apparatus. During the period of force maintenance, phenylephrine produces a larger ratio of force to light than does K+ depolarization. The maintenance of force in the presence of either phenylephrine or elevated K+ requires an elevation of intracellular Ca2+ levels above base-line values. These results suggest that phenylephrine can increase the effectiveness of Ca2+ on the contractile apparatus.