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Calcium dependency and the effect of calcium antagonists on molluscan proboscis smooth muscles from the whelk, Buccinum undatum.

Research output: Contribution to Journal/MagazineJournal articlepeer-review

  • I. D. Nelson
<mark>Journal publication date</mark>06/1994
<mark>Journal</mark>Journal of Comparative Physiology B
Issue number2
Number of pages9
Pages (from-to)147-155
Publication StatusPublished
<mark>Original language</mark>English


In all four proboscis muscles of the whelk Buccinum undatum, the potassium-induced depolarization response was acutely dependent upon extracellular calcium, being eliminated in calcium-free conditions. The responses to acetylcholine were found to be partly dependent upon intracellular calcium. Responses to the peptides phenylalanine-methionine-arginine-phenylalanine-NH2 and phenylalanine-leucine-arginine-phenylalanine-NH2 were much more resistant to calcium-free conditions and appeared to engage the excitation-contraction coupling mechanism by mobilizing stored intracellular calcium. Sucrose-gap studies of radular retractor muscles showed that the organic calcium “antagonist” nifedipine enhanced potassium-induced depolarization responses, initiating spike-like action potentials and associated fast twitch activity. The inorganic calcium antagonist gadolinium exerted concentration-dependent inhibitory actions on these muscles. Basal tonus and fast twitch activity in response to potassium-induced depolarization were eliminated as were the spike-like action potentials of the membrane electrical response. The inorganic calcium “antagonist” cadmium greatly enhanced potassium-induced contractures in all four muscles, and on its own it induced tonic force and fast twitches in all the muscles. It seems likely that cadmium may have displaced stored intracellular calcium to induce myofilament activation. While these molluscan smooth muscles appear to possess calcium channels with fast and slow characteristics, their behaviour and pharmacological manipulation is very different from their more well known mammalian transient and long-lasting channel counterparts.