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The mechanisms by which high-K+ saline and acetylcholine (ACh) mobilize cellular calcium in molluscan muscle was studied in three proboscis muscles of Busycon canaliculatum. BAY K 8644, a calcium agonist, enhanced tonic force induced by exposure to 25 mmoll−1 K+ in the odontophore and radular retractor muscles but inhibited this response in the radular sac muscle. Its effect on the radular protractor muscle was concentration-dependent, excitatory at 10−7 mol l−1 and inhibitory at higher concentrations. The tonic response to 80 mmoll−1 1 K+ was enhanced by BAY K 8644 in the odontophore retractor and radular retractor muscles but inhibited in the radular sac muscle. In all muscles, BAY K 8644 eliminated the fast twitches induced by 80 mmolI−1 K+, and inhibited the tonic ACh responses. Sucrose-gap studies with the radular protractor muscle showed that the effects of BAY K 8644 on the depolarizations induced by K+ and ACh were similar. The effect on the ACh-induced depolarization suggested that this agent had inhibited sodium influx through the ACh receptor.

Mytelase enhanced ACh-induced tonic force, but at 10−4moll−1 it inhibited the response to doses of ACh above 10−5moll−1. Mytolon reduced the maximum ACh-induced tonic force and increased the response threshold to ACh. ACh and high-K+ depolarization pathways were not synergistic for force development

The existence of two separate cellular calcium pools, independently released by high-K+ saline and ACh, seems improbable. We suggest that K+ and ACh act via separate mechanisms to release calcium from a single cellular calcium pool.