Application of Ca2+ (0.1-2.5 mM) to guinea pig aortas incubated in Ca(2+)-free isotonic KCl solution induced a contraction (Ca contraction), a part of which depended on preloading the intracellular stores with Ca2+ and which was sensitive to 3 x 10(-5) M ryanodine. Because 45Ca2+ influx from the external fluid upon the addition of Ca2+ was not modified either by the state of filling of the Ca2+ store or by the presence of ryanodine, the ryanodine-sensitive component of the contraction could be attributed to the Ca2+ influx-induced Ca2+ release from the Ca2+ store. Supporting the possibility of involvement of Ca(2+)-induced Ca2+ release, the Ca contraction due to 0.1 mM Ca2+ was enhanced either by decreasing Mg2+ in the medium or by low temperature. The ratio of the ryanodine-sensitive fraction in the Ca contraction was inversely related to the concentration of Ca2+ added and also to the extent of 45Ca2+ influx. When the Ca2+ influx was decreased by verapamil or cadmium, the ratio of ryanodine-sensitive fraction increased. On the contrary, an increase of Ca2+ influx by CGP-28392 decreased the ratio. These results suggest that Ca2+ influx at a physiological level triggers Ca2+ release from the Ca2+ store, resulting in the amplification of contractile force.