Converting gallbladder absorption to secretion: the role of intracellular calcium.

Abstract

BACKGROUND:

Experimental cholelithiasis is associated with elevated biliary calcium concentration and altered gallbladder absorption. Recent studies showed that extracellular calcium ([Ca2+]ec) plays a role in regulating gallbladder ion transport. The extent to which intracellular calcium ([Ca2+]ic) mediates the changes in gallbladder ion transport is not clear. We hypothesize that [Ca2+]ic is an important regulator of gallbladder ion transport.

METHODS:

Prairie dog gallbladders were mounted in Ussing chambers, standard electrophysiologic parameters were recorded, and unidirectional Na+, Cl- and H2O fluxes were measured before and after mucosal exposure of 10-5 mol/L calcium ionophore A23187 was performed.

RESULTS:

A23187 caused an increase in transepithelial short-circuit current and potential difference and a decrease in transepithelial resistance. A23187 inhibited mucosa to serosa Cl- flux and stimulated serosa to mucosa Na+ flux, resulting in increased net Cl- secretion and decreased net Na+ absorption. A23187 converted H2O from absorption to secretion. Transepithelial short-circuit current effect of A23187 was delayed by indomethacin pretreatment and was completely blunted by low bathing Ca2+.

CONCLUSIONS:

This is the first demonstration that increased [Ca2+]ic converts the gallbladder from its normal absorptive state to a secretory one. Furthermore [Ca2+]ic appears to regulate ion transport through mechanisms that are partially prostaglandin-dependent. Studies are necessitated to define possible links between gallbladder secretion of Cl- and H2O and mucus hypersecretion, a well-described phenomenon associated with cholesterol gallstone formation.

• Authors: A J Moser, M Z Abedin, J A Cates, D I Giurgiu, J A Karam, J J Roslyn
• Journal: Surgery (Surgery) Vol. 119 Issue 4 Pg. 410-6 (Apr 1996) ISSN: 0039-6060 [Print] United States
• PMID: 8644006 (Publication Type: Journal Article, Research Support, U.S. Gov't, Non-P.H.S.)

Chemical References

• Chlorides
• Calcimycin
• Sodium
• Cyclic AMP
• Calcium
• Indomethacin

Topics

• Animals
• Calcimycin (pharmacology)
• Calcium (physiology)
• Chlorides (metabolism)
• Cholelithiasis (metabolism)
• Cyclic AMP (physiology)
• Dogs
• Gallbladder (metabolism)
• Indomethacin (pharmacology)
• Male
• Sodium (metabolism)