1. Noradrenaline 1 microM induced a contractile response in rat isolated aorta in the presence or in the absence of extracellular Ca2+ with depletion of intracellular Ca2+ stores. Thereafter, during incubation in the presence of Ca2+, an increase in the resting tone was observed. Such a contractile response did not occur after exposure to caffeine or 5-hydroxytryptamine. 2. This increase in tension was inhibited in a concentration-dependent manner by alpha-adrenoceptor antagonists (prazosin, phentolamine and yohimbine), the non-specific relaxing compound, papaverine and by the Ca(2+)-entry blocker, nifedipine. Therefore, this contractile process is related to depletion of Ca2+ stores sensitive to noradrenaline and is linked to Ca2+ entry through voltage-operated Ca2+ channels and alpha-adrenoceptors. 3. Phentolamine and yohimbine did not block the Ca2+ refill pathway; prazosin and nifedipine inhibited the reuptake of Ca2+ by an internal store sensitive only to noradrenaline; papaverine inhibited the refilling of caffeine- and noradrenaline-sensitive Ca(2+)-stores.