The mechanism of spontaneous contraction of vascular smooth muscles in the elastic artery was studied in a ring-shaped preparation isolated from the rat aorta. The observation of small changes in vascular tension with a high gain AC amplification of tension signal provided a reliable detection of spontaneous contractions. The spontaneous rhythmic contraction (RC) occurred consistently in the preparation taken from the thoracic aorta without external stimuli. The RC (frequency, 5-20 cycle/min; amplitude, 10-100 mg) was accompanied with small oscillatory changes in the membrane potential (2-5 mV, peak to peak). A reduction in temperature (below 30 degrees C) or superfusing the preparation with Ca-free solution inhibited the generation of RC. Ca-entry blockers (verapamil and nifedipine) also inhibited the RC. The cessation of RC by these procedures reduced the vascular tension by about 40% of control baseline tension. The application of adrenergic blockers had little effect on the pattern of RC and on the vascular tension. The results suggest that the RC is generated by a synchronization of electrical and mechanical activities in relatively small groups of smooth muscle cells, which depends upon the temperature and requires the Ca-entry into the cells. The process of initiation of spontaneous RC in the rat aorta was discussed.