The process of tension repriming and the phenomenon of tension potentiation after premature stimulation (post-extrasystolic potentiation, PESP) were studied in the adult guinea pig atrium. The following results were obtained. (i) Reducing extracellular calcium, [Ca]o, to 50% of normal did not significantly change the rate of tension repriming. However, in the presence of 5 microM isoprenaline (which greatly speeded up repriming) the same reduction in [Ca]o slowed down the repriming process. (ii) Increases in the rate of stimulation enhanced the rate of tension repriming in a control medium, but this rate-dependence was absent in the presence of isoprenaline. (iii) Isoprenaline (20 microM) abolished PESP. A reduction in [Ca]o or the addition of verapamil (still with isoprenaline) partly restored tension potentiation. In neonatal guinea pig atria, a large PESP was evident, which was only slightly reduced by isoprenaline. These results are interpreted as reflecting changes induced by isoprenaline in the degree of filling of sarcoplasmic reticulum (SR) stores with calcium, and in the rate of calcium recycling between uptake and release sites within the SR network. The large PESP found in the neonate, and its relative insensitivity to isoprenaline was interpreted as reflecting a scarcity of SR. This implies that tension potentiation may also reflect changes in sarcolemmal calcium currents.