Sodium ion transport participates in non-neuronal acetylcholine release in the renal cortex of anesthetized rabbits

Shuji Shimizu, Tsuyoshi Akiyama, Toru Kawada, Yusuke Sata, Michael James Turner, Masafumi Fukumitsu, Hiromi Yamamoto, Atsunori Kamiya, Toshiaki Shishido, Masaru Sugimachi

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This study examined the mechanism of release of endogenous acetylcholine (ACh) in rabbit renal cortex by applying a microdialysis technique. In anesthetized rabbits, a microdialysis probe was implanted into the renal cortex and perfused with Ringer’s solution containing high potassium concentration, high sodium concentration, a Na+/K+-ATPase inhibitor (ouabain), or an epithelial Na+ channel blocker (benzamil). Dialysate samples were collected at baseline and during exposure to each agent, and ACh concentrations in the samples were measured by high-performance liquid chromatography. High potassium had no effect on renal ACh release. High sodium increased dialysate ACh concentrations significantly. Ouabain increased dialysate ACh concentration significantly. Benzamil decreased dialysate ACh concentrations significantly both at baseline and under high sodium. The finding that high potassium-induced depolarization does not increase ACh release suggests that endogenous ACh is released in renal cortex mainly by non-neuronal mechanism. Sodium ion transport may be involved in the non-neuronal ACh release.

Original languageEnglish
Pages (from-to)587–593
Number of pages7
JournalJournal of Physiological Sciences
Issue number5
Publication statusPublished - Sep 2017
Externally publishedYes


  • Acetylcholine
  • Microdialysis
  • Non-neuronal release
  • Renal cortex
  • Sodium

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