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Nitric oxide and gall-bladder motor function

W Luman1, J E Ardill, E Armstrong

  • 1Gastrointestinal Unit, Western General Hospital, Edinburgh, Scotland, UK.

Alimentary Pharmacology & Therapeutics
|July 15, 1998
PubMed
Summary
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Nitric oxide (NO) donors relax gallbladder smooth muscle but impair gallbladder emptying. While NO influences motility, nitric oxide synthase (NOS) is unlikely to be the neurotransmitter for nonadrenergic noncholinergic (NANC) gallbladder innervation.

Area of Science:

  • Gastroenterology
  • Physiology
  • Pharmacology

Background:

  • The L-arginine: nitric oxide (NO) pathway is crucial for intestinal motility regulation.
  • NO is a potential mediator for nonadrenergic noncholinergic (NANC) neurotransmission.

Purpose of the Study:

  • To investigate the role of the L-arginine: NO pathway in gallbladder motor function.
  • To determine if NO influences gallbladder contraction and emptying.

Main Methods:

  • In vitro studies used bovine and human gallbladder strips stimulated with cholecystokinin (CCK).
  • Effects of NO donors (GTN, SNP) and NOS inhibitor (L-NMMA) on muscle contraction were assessed.
  • In vivo studies in healthy volunteers measured postprandial gallbladder emptying during infusions of NO donors, L-NMMA, and controls.

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Main Results:

  • NO donors (GTN, SNP) relaxed CCK-stimulated gallbladder muscle in vitro.
  • L-NMMA increased basal gallbladder muscle tone in vitro.
  • In vivo, NO donors significantly impaired gallbladder emptying, while L-NMMA did not affect emptying.
  • Immunohistochemistry for NOS was negative in human gallbladders.

Conclusions:

  • Pharmacological doses of NO donors impair gallbladder emptying and relax smooth muscle.
  • Despite NO's effect on motility, the absence of NOS suggests it's not the primary neurotransmitter for NANC gallbladder innervation.