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[Exogenous nitric oxide and gallbladder contractility in humans].

Stefan Bednarz1, Teresa Pawlik, Kazimierz Janicki

  • 1Katedra Chorób Wewnetrznych i Gerontologii Collegium Medicum Uniwersytetu Jagiellońskiego w Krakowie.

Przeglad Lekarski
|January 9, 2003
PubMed
Summary

Exogenous nitric oxide (NO) donors like glyceryl trinitrate and molsidomine increase fasting gallbladder volume and inhibit meal-stimulated gallbladder contraction in healthy adults. These findings confirm NO

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Area of Science:

  • Gastroenterology
  • Physiology
  • Pharmacology

Context:

  • The gallbladder (GB) concentrates and delivers bile, requiring coordinated motor, secretory, and absorptive functions.
  • Nitric oxide (NO) acts as an intrinsic neurotransmitter in nonadrenergic, noncholinergic (NANC) pathways, inhibiting GB tone and contraction.

Purpose:

  • To investigate the effects of exogenous NO donors (glyceryl trinitrate, molsidomine, L-arginine) on fasting GB volume and post-meal gallbladder contraction (ejection fraction).

Summary:

  • Healthy subjects received GTN, MO, or L-arginine. GTN and MO significantly increased fasting GB volume and reduced post-prandial ejection fraction.
  • L-arginine did not affect resting GB volume but significantly reduced stimulated ejection fraction.
  • These findings confirm NO's potent inhibitory effect on human gallbladder motor activity.

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Impact:

  • Demonstrates that exogenous NO donors can modulate gallbladder function.
  • Provides evidence for the role of NO in regulating gallbladder motor activity.
  • Suggests potential therapeutic targets for conditions involving gallbladder dysmotabolism.