title: Ionic dependency of membrane potential and autorhythmicity in the atrium of the whelk Busycon canaliculatum.
abstract: 1. Calcium-free media usually caused a cessation of all electrical and mechanical activity of the Busycon atrium. Where any electrical activity survived, the action potential consisted of a pre- and plateau-like potential devoid of the usual terminal spike. 2. High Ca salines induced tonic force, membrane depolarization and reduction in generation of spontaneous action potentials. The Ca ionophore A23187 enhanced contractions and the SR CaATPase inhibitor cyclopiazonic acid induced slight depolarization, tonic contractures and increased action potential firing. 3. The inorganic Ca antagonist Co2+ was without effect on the preparations, although the lanthanide Gd3+ inhibited contractions and spontaneous action potentials as well as inducing membrane potential depolarization. 4. The organic Ca entry-blocker nifedipine enhanced both spontaneous action potential amplitude and the phasic contractions they generated. 5. High K salines considerably depolarized atrial preparations with accompanying large tonic contractures and suppression of action potentials. The K channel-blocker 4AP enhanced action potential amplitude with slight increase in contractions, and TEA depolarized the atrium, and enhanced action potentials and rhythmic contractions. 6. Sodium-free salines strongly hyperpolarized atrial preparations and abolished spontaneous action potentials and, on washout, the membrane potential became temporarily unstable. In 2 preparations, low chloride and chloride-free media induced significant membrane potential hyperpolarization. 7. It is concluded that, in the atrium, the resting membrane potential is largely determined by the transmembrane K gradient, but with significant conductances to Na and Cl though probably not Ca. The action potential spike appears to be a Ca-dependent event and the plateau-like phase may be a Na-dependent event.
authors.affiliation: Division of Biological Sciences, Lancaster University, U.K.
authors.forename: H
authors.initials: H
authors.lastname: Huddart
authors.forename: R B
authors.initials: RB
authors.lastname: Hill
mesh_terms: D000200:Action Potentials / Q000187:drug effects / Q000502:physiology; D000818:Animals; D016275:Atrial Function; D002118:Calcium / Q000502:physiology; D002121:Calcium Channel Blockers / Q000494:pharmacology; D002712:Chlorides / Q000494:pharmacology; D006321:Heart / Q000187:drug effects / Q000502:physiology*; D006325:Heart Atria / Q000187:drug effects; D006706:Homeostasis / Q000187:drug effects / Q000502:physiology; D066298:In Vitro Techniques; D007476:Ionophores / Q000494:pharmacology; D008564:Membrane Potentials / Q000187:drug effects / Q000502:physiology; D008974:Mollusca / Q000502:physiology*; D009200:Myocardial Contraction / Q000187:drug effects / Q000502:physiology; D011188:Potassium / Q000494:pharmacology; D012964:Sodium / Q000494:pharmacology
chemical_list: D002121:Calcium Channel Blockers; D002712:Chlorides; D007476:Ionophores; D012964:Sodium; D011188:Potassium; D002118:Calcium