title: Non-neuronal expression of choline acetyltransferase in the rat kidney.
abstract: OBJECTIVE
  Acetylcholine (ACh) has been shown to increase ion and water excretion in the kidneys, resulting in hypotension. However, no evidence of renal parasympathetic innervation has been shown, and the source of ACh acting on nephrons is still unknown. The aim of the present study was to identify ACh-producing cells in the rat kidney, by examining the expression of cholinergic agents and localization of an ACh-synthesizing enzyme, choline acetyltransferase (ChAT), in the kidney.
  
  
  METHODS
  Adult mail Sprague-Dawley rats were used in this study. Expression of mRNA of cholinergic agents, ChAT, vesicular ACh transporter (VAChT), and high-affinity choline transporter (CHT-1), in the kidney was examined by RT-PCR. Localization of ChAT mRNA and protein was examined by in situ hybridization and tyramide-enhanced immunohistochemistry, respectively.
  
  
  RESULTS
  RT-PCR showed the expression of ChAT, VAChT, and CHT-1. In situ hybridization demonstrated that ChAT mRNA is localized to the renal cortical collecting ducts (CCD). Immunohistochemistry showed that the ChAT-positive cells were principal cells, and that they were unevenly distributed in the tubules, and constituted approximately 15.2% of CCD in the cortex, and 3.6% and 1.5% in the outer and inner medulla, respectively. ChAT-positive immunoreactivity was localized to the apical side of principal cells, suggesting that ACh synthesis may occur in the apical compartment of these cells.
  
  
  CONCLUSIONS
  These results suggest that the cholinergic effects in the nephron may be mediated at least in part by ACh originating from CCD principal cells and its expression may be locally regulated in the rat kidney.
authors.affiliation: Department of Anatomy and Cell Biology, Hyogo College of Medicine, 1-1 Mukogawa, Nishinomiya, Hyogo 663-8501, Japan. maedas@hyo-med.ac
authors.forename: Seishi
authors.initials: S
authors.lastname: Maeda
authors.forename: Jin Gon
authors.initials: JG
authors.lastname: Jun
authors.forename: Sachi
authors.initials: S
authors.lastname: Kuwahara-Otani
authors.forename: Koichi
authors.initials: K
authors.lastname: Tanaka
authors.forename: Tetsu
authors.initials: T
authors.lastname: Hayakawa
authors.forename: Makoto
authors.initials: M
authors.lastname: Seki
mesh_terms: D000109:Acetylcholine / Q000378:metabolism*; D000818:Animals; D001921:Brain / Q000378:metabolism; D002795:Choline O-Acetyltransferase / Q000378:metabolism*; D007150:Immunohistochemistry; D007668:Kidney / Q000201:enzymology* / Q000378:metabolism; D007672:Kidney Cortex / Q000201:enzymology*; D007685:Kidney Tubules, Collecting / Q000166:cytology / Q000201:enzymology*; D008297:Male; D026901:Membrane Transport Proteins / Q000235:genetics / Q000378:metabolism; D009474:Neurons / Q000201:enzymology* / Q000378:metabolism; D012313:RNA / Q000378:metabolism; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D050494:Vesicular Acetylcholine Transport Proteins / Q000235:genetics / Q000378:metabolism
chemical_list: D026901:Membrane Transport Proteins; D012333:RNA, Messenger; D050494:Vesicular Acetylcholine Transport Proteins; C065637:choline transporter; D012313:RNA; D002795:Choline O-Acetyltransferase; D000109:Acetylcholine