1. In a Ca2+-free medium caffeine (10 mM) was still able to cause a phasic contraction in rabbit iliac arteries. 2. Bay K 8644 at 10(-6) but not at 10(-7) M potentiated the residual response to caffeine in a Ca2+-free medium. In a Ca2+-free medium with or without KCl (40 mM), Bay K 8644, however, caused no contraction. 3. Nifedipine (10(-6) M) did not affect the residual caffeine-response or the potentiating effect of Bay K 8644. Verapamil (10(-6) M), however, inhibited both the caffeine response and the potentiation. 4. Bay K 8644 (10(-6) M) potentiated the contractile response to Ca2+ (0.01-2.4 mM) in a Ca2+-free medium containing KCl. The potentiation was equally inhibited by nifedipine or verapamil. 5. La#+ (1 mM), EGTA (0.1 mM), or vanadate (10(-4) M) completely inhibited the Bay K 8644-induced potentiation without affecting the residual caffeine response. 6. These results suggest that the potentiating action of Bay K 8644 on the residual caffeine response in a Ca2+-deficient medium may not be related to voltage-dependent Ca2+ channels. In addition, the activity of Ca2+-ATPase in sarcolemmal membranes may be important in this potentiation.