Nerve-induced contractions of rat isolated vas deferens were examined to determine how the rapid and slow twitch phases summate to produce the two-component tetanus. The rapid phase (time to peak, 200-300 ms) had a latency of 35-50 ms and was selectively abolished by nifedipine but not verapamil. The slow phase (time to peak, 500-650 ms), as seen in the presence of nifedipine, had a latency of 100-200 ms. During a train of pulses at 0.5-2 Hz, its size declined rapidly and its latency lengthened. The rapid phase responses at these frequencies were progressively potentiated to a peak after 12-40 s, a time similar to the peak of the secondary tetanic component at 5 Hz. Doses of verapamil which abolished both this potentiation and the secondary tetanic component did not block the slow twitch phase. The results indicate that the primary tetanic component is a summation of 'non-adrenergic' (rapid phase) and direct adrenergic (slow phase) contractions. In contrast the secondary increase in tetanic tension results largely from the alpha 1-adrenoceptor induced potentiation of the rapid non-adrenergic twitch mechanism. The mechanisms for the two phases and for the potentiation each appear to involve different calcium sources.