Home > Research > Publications & Outputs > The calcium dependence of electrical and mechan...
View graph of relations

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

Research output: Contribution to Journal/MagazineJournal article

  • H. Huddart
  • I. D. Nelson
  • D. D. Brooks
  • R. B. Hill
<mark>Journal publication date</mark>06/1992
<mark>Journal</mark>Comparative Biochemistry and Physiology Part A: Physiology
Issue number2
Number of pages7
Pages (from-to)299-305
Publication StatusPublished
<mark>Original language</mark>English


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. Co2+, Cd2+ and Gd3+ all inhibited the ACh and K+ responses of the OP muscle but Gd3+ was the most consistent and potent inhibitor of these responses. 5. 5. Gd3+ 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.