Nitric oxide and gallbladder motility in prairie dogs

Howard Salomons, Andrew P. Keaveny, Robert Henihan, Gwynneth Offner, Ashok Sengupta, Wayne W. Lamorte, Nezam H. Afdhal

Research output: Contribution to journalArticlepeer-review

19 Scopus citations


In this study we evaluated the role of nitric oxide (NO) on gallbladder motility in the normal prairie dog by 1) immunohistochemistry, 2) an enzymatic assay for NO synthase (NOS), and 3) an in vivo model to measure whole gallbladder tone and contractility. NOS was localized to gallbladder mucosal cells by NADPH-diaphorase and polyclonal antibodies to a constitutive brain NOS. Gallbladder mucosal homogenates demonstrated total NOS activity in the range of 578 ± 115 pmol · mg protein-1 · 30 min-1. Blockade of NOS activity in vivo using Nω-nitro-L-arginine methyl ester resulted in an up to 80% increase in gallbladder tone from basal. A 40% increase in tone was seen with methylene blue, suggesting that tone was maintained by both NO activation of guanylate cyclase and possibly direct effects on Ca2+ channels. An exogenous nitrosothiol, S-nitroso-N-acetyl-cysteine, abolished cholecystokinin (CCK) octapeptide and bethanechol-stimulated gallbladder contraction. We conclude that the prairie dog gallbladder contains constitutive NOS and synthesizes NO, which is important for the maintenance of basal gallbladder tone and is an inhibitor of the contractile response of the gallbladder to agonists such as CCK and bethanechol.

Original languageEnglish (US)
Pages (from-to)G770-G778
JournalAmerican Journal of Physiology - Gastrointestinal and Liver Physiology
Issue number4 35-4
StatePublished - Apr 1997


  • cholecystokinin
  • cholelithiasis
  • guanosine 3',5'-cyclic monophosphate
  • smooth muscle

ASJC Scopus subject areas

  • Physiology
  • Hepatology
  • Gastroenterology
  • Physiology (medical)


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