The calcium dependence of electrical and mechanical responses of the odontophore protractor muscle of Busycon canaliculatum. A sucrose-gap study of calcium antagonist action

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1. 1. Exposures for 30 min to Ca-free salines irreversibly inhibited responses of the odontophore protractor (OP) muscles of Busycon canaliculatum to ACh and high K + salines. Under continuous field stimulation, Ca-free salines extinguished the responses within 3 min and recovery on Ca readmission was only partial. 2. 2. Nifedipine converted normally smooth ACh-induced depolarizations into oscillatory events generating small twitch-like contractions. 3. 3. Nifedipine converted normally tonic high K + responses into depolarizations with fast spike-like action potentials generating fast twitches. The low K +induced action potentials and fast twitches of this muscle were greatly enhanced by nifedipine. Nifedipine induced rapid transient inward current pulses accompanying this twitch activity. 4. 4. Co 2+, Cd 2+ and Gd 3+ all inhibited the ACh and K + responses of the OP muscle but Gd 3+ was the most consistent and potent inhibitor of these responses. 5. 5. Gd 3+ did not affect K +- or ACh-induced depolarization levels but eliminated spike-like action potentials and the twitches they generated. 6. 6. When the muscle membranes were depolarized with increasing K + subsequent ACh responses were inhibited and eventually eliminated at about −41 mV, indicating that the ACh receptor here showed voltage inactivation. 7. 7. Although dependent upon an influx of[Ca] 0 for CIRC to effect EC coupling, this Ca appears to enter the cells by a mechanism unlike that of mammalian smooth muscle. The cellular Ca pool appears to be independently but not synergistically accessed by ACh and K + in the induction of contractile responses.