Muscarinic acetylcholine receptor compounds alter net Ca2+ flux and contractility in an invertebrate smooth muscle

Constance Leah Devlin, William Arnole, Shawn Anderson, Kyle Shea

Research output: Contribution to journalArticlepeer-review

5 Scopus citations

Abstract

Responses of a holothurian smooth muscle to a range of muscarinic (M 1 to M5) acetylcholine receptor (mAChR) agonists and antagonists were surveyed using calcium (Ca2+)-selective electrodes and a mechanical recording technique. Most of the mAChR agonists and antagonists tested increased both contractility and net Ca2+ efflux, with M1-specific agents like oxotremorine M being the most potent in their action. To investigate the possible sources of Ca2+ used during mAChR activation, agents that disrupt intracellular Ca2+ ion sequestration [cyclopiazonic acid (CPA), caffeine, ryanodine], the phosphoinositide signaling pathway [lithium chloride (LiCl)], and L-type Ca 2+ channels (diltiazem and verapamil) were used to challenge contractions induced by oxotremorine M. These contractions were blocked by treatment with CPA, caffeine, LiCl, and by channel blockers, diltiazem and verapamil, but were unaltered by ryanodine. Our data suggest that this smooth muscle had an M1,3,5-like receptor that was associated with the phosphoinositide signaling pathway that relied on intracellular Ca2+ stores, but secondarily used extracellular Ca2+ via the opening of L-type channels.

Original languageEnglish (US)
Pages (from-to)9-17
Number of pages9
JournalInvertebrate Neuroscience
Volume5
Issue number1
DOIs
StatePublished - Nov 1 2003

All Science Journal Classification (ASJC) codes

  • Developmental Neuroscience
  • Cellular and Molecular Neuroscience

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