Exposure of the rabbit abdominal aorta to the combination of high K+ and norepinephrine resulted in a time-dependent increase in the rate of 45Ca influx and 45Ca and 22Na content over that observed after stimulation with either K+ or norepinephrine alone. The increase in 45Ca influx, but not the increase in 22Na content, was extracellular Ca2+ (Cao2+) dependent. This time-dependent increase in 45Ca influx was prevented by incubating the tissue in Na(+)-free medium. Nifedipine inhibited both the initial depolarization-induced 45Ca influx and time-dependent increase in 45Ca influx and 22Na content. The effect of nifedipine on time-dependent fluxes was prevented by ouabain. Phorbol dibutyrate mimicked the effects of norepinephrine on 22Na retention and 45Ca fluxes. The effects of phorbol dibutyrate and norepinephrine were not additive. It is concluded that, in rabbit abdominal aorta, norepinephrine plus K+ causes 22Na retention (possibly through inhibition of the sodium pump) and a Cao(2+)- and intracellular Na+ (Nai+)-dependent increase in 45Ca influx. This latter effect is possibly the result of increased Nai(+)-Cao2+ exchange.