Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5 Pt 1
pubmed:dateCreated
1989-6-16
pubmed:abstractText
Bile formation by the liver is largely dependent on the transport of bile acids by hepatocytes. This process is thought to result from Na-coupled uptake of bile acids into the cell and voltage-dependent, carrier-mediated transport from cell to canaliculus. However, the dependence of bile secretion on membrane potential has not yet been observed. In this study, the effect of changes in membrane potential differences on bile secretion was tested by impaling rat hepatocyte couplets with microelectrodes, changing membrane potential by intracellular current injection, and measuring fluid secretion by optically determining canalicular size. In the presence of 50 microM taurocholate, membrane potential was -33.3 +/- 5.8 mV and canalicular area increased by 6 +/- 6%/min, corresponding to a fluid secretion rate of 2-4 fl/min. In contrast, when intracellular voltage was suddenly changed to -109.9 +/- 15.0 mV, the canalicular area increased by 20 +/- 4%/min, corresponding to a secretion rate of 19 fl/min. When these experiments were repeated in the absence of taurocholate, the negative clamp had no effect on canalicular size. Taurocholate itself did not alter membrane potential. These findings support the hypothesis that canalicular bile secretion depends on a process equivalent to electrodiffusion. We therefore conclude that membrane voltage is a driving force for taurocholate-dependent fluid secretion by the liver.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0002-9513
pubmed:author
pubmed:issnType
Print
pubmed:volume
256
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
G826-32
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1989
pubmed:articleTitle
Voltage-driven, taurocholate-dependent secretion in isolated hepatocyte couplets.
pubmed:affiliation
Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut 06510.
pubmed:publicationType
Journal Article, In Vitro, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't