The role of the passive Ca²⁺ trap (Bradley et al., in press) in limiting the amplitude of contraction following Ca²⁺ influx was examined in intact pieces of colon from guinea pigs (∼ 500 g, humanely killed by stunning then immediate exsanguination). Contraction by Ca²⁺ influx was induced by KCl (30 mM) depolarisation and measured conventionally using a force-tension transducer and Grass polygraph in the presence of atropine, phentolamine and mepyramine (all at 1 µM to inhibit the activity of neurotransmitters released by nerve depolarisation). Ryanodine (50 µM), following brief applications of caffeine (10 mM, which was washed out in the continuous presence of ryanodine) to open ryanodine receptors (RyR), enhanced KCl-induced contractions significantly (control 23 ± 3 mN, in ryanodine 63 ± 4 mN, n=9, p<0.05; mean ± sem, statistical analysis was determined by paired Student’s t-tests, where p<0.05 was considered significant) as predicted from disruption of the Ca²⁺ trap. The RyR blocker tetracaine prevented the increase in the amplitude of KCl-induced contractions produced by ryanodine. Upon washout of tetracaine, the ability of ryanodine to increase KCl-induced contractions was restored. Cyclopiazonic acid (CPA) itself, which inhibits the SR Ca²⁺ pump, induced contractions that were blocked by the voltage-dependent Ca²⁺ channel blocker nimodipine (1 µM). This result suggests CPA-induced contractions were mediated via voltage-dependent Ca²⁺ channels. CPA-evoked Ca²⁺ influx is probably due to depletion of the SR and the ensuing inhibition of the negative feedback pathway, which under control conditions hyperpolarises the membrane potential and prevents Ca²⁺ influx (Nelson et al., 1995). Tetracaine (100 µM) reduced the amplitude of CPA-induced contractions by inhibiting RyR even under conditions where the SR was depleted of Ca²⁺.Together these results suggest that open RyR facilitate the entry of Ca²⁺ to the bulk of the cytoplasm to evoke contraction. Previous results from single colonic myocytes revealed that the closely apposed regions of the SR and sarcolemma form a passive Ca²⁺ trap independent of SR Ca²⁺ pump activity which restricts the movement of Ca²⁺ to the deeper myoplasm following Ca²⁺ influx (Bradley et al., in press). Present results from intact tissue show that under physiological conditions a passive Ca²⁺ trap restricts the access of incoming Ca²⁺ to the contractile machinery.