AJP - GI Watch the video to learn how APS reaches out to developing nations.
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Am J Physiol Gastrointest Liver Physiol 252: G699-G706, 1987;
0193-1857/87 $5.00
This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Fitz, J. G.
Right arrow Articles by Scharschmidt, B. F.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Fitz, J. G.
Right arrow Articles by Scharschmidt, B. F.

AJP - Gastrointestinal and Liver Physiology, Vol 252, Issue 5 699-G706, Copyright © 1987 by American Physiological Society

ARTICLES

Intracellular chloride activity in intact rat liver: relationship to membrane potential and bile flow

J. G. Fitz and B. F. Scharschmidt

Active chloride transport has been described in a variety of epithelia, and intracellular chloride activity (aiCl) in these tissues is generally elevated twofold or more above the level predicted for passive diffusion. To determine whether active chloride transport might contribute to canalicular bile formation, we have used conventional and Cl- -selective microelectrodes to measure aiCl of rat hepatocytes in vivo under a variety of conditions. Under basal conditions, the membrane potential difference averaged -33.2 +/- 3.5 mV (means +/- SD) in 29 animals, and the ratio (R) of observed aiCl (24.8 mM) to that expected for passive distribution at this membrane potential (22.6 mM) was 1.10 +/- 0.08, a value slightly but significantly greater than that predicted for passive distribution. Infusion of alanine (45-mumol bolus, 10.8-mumol/min infusion) in 5 animals hyperpolarized the membrane potential to -43.6 +/- 4.0 mV over 10-15 min and resulted in a significant fall in aiCl to 15.1 +/- 4.8 mM but with no change in R. Infusion of theophylline (577 nmol/min), taurocholate (3-mumol bolus, 810-nmol/min infusion), and ursodeoxycholic acid (4-mumol bolus, 2.13-mumol/min infusion) into 5 animals each increased bile flow by 6.1, 34.1, and 96.8%, respectively, compared with saline-infused controls but did not alter membrane potential or chloride distribution. These observations indicate that aiCl is close to the level predicted for passive distribution under basal conditions, after hyperpolarization of the membrane potential by alanine, and after stimulation of bile flow by a variety of choleretics. By analogy with Cl- -secreting epithelia, it appears unlikely that active chloride transport across the basolateral membrane contributes significantly to canalicular bile formation by the hepatocyte.


This article has been cited by other articles:


Home page
 Am. J. Physiol. Gastrointest. Liver Physiol.Home page
S. D. Lidofsky and R. M. Roman
Alanine uptake activates hepatocellular chloride channels
Am J Physiol Gastrointest Liver Physiol, October 1, 1997; 273(4): G849 - G853.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online