Enhancing effects of vasoconstrictors on bile flow and bile acid excretion in the isolated perfused rat liver

The effects of aniso-osmotically and amino-acid-induced cell-volume changes on bile flow and biliary taurocholate excretion were studied in isolated perfused rat liver. With taurocholate (100 microM) in the influent perfusate, hypo-osmotic exposure (225 mosmol/l) increased taurocholate excretion into bile and bile flow by 42 and 27% respectively, whereas inhibition by 32 and 47% respectively was observed after hyperosmotic (385 mosmol/l) exposure. The effects of aniso-moticity on taurocholate excretion into bile was observed throughout aniso-osmotic exposure, even after completion of volume-regulatory ion fluxes and were fully reversible upon re-exposure to normo-osmotic media. Hypo-osmotic cell swelling (225 mosmol/l) increased the Vmax. of taurocholate translocation from the sinusoidal compartment into bile about 2-fold. Also, cell swelling induced by glutamine and glycine stimulated both bile flow and biliary taurocholate excretion. There was a close relationship between the aniso-osmotically and amino-acid-induced change of cell volume and taurocholate excretion into bile. The data suggest that liver cell volume plays an important role in regulating bile-acid-dependent bile flow and biliary taurocholate excretion.

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Endothelin-1 stimulates bile acid secretion and vesicular transport in the isolated perfused rat liver

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.1994.266.2.g324 ◽

1994 ◽

Vol 266 (2) ◽

pp. G324-G329 ◽

Cited By ~ 3

Author(s):

A. Tanaka ◽

K. Katagiri ◽

M. Hoshino ◽

T. Hayakawa ◽

K. Tsukada ◽

...

Keyword(s):

Bile Acid ◽

Rat Liver ◽

Bile Flow ◽

Low Dose ◽

Portal Pressure ◽

Vesicular Transport ◽

Bile Secretion ◽

Isolated Perfused Rat Liver ◽

High Dose ◽

Perfused Rat Liver

The effects of endothelin (ET) on portal pressure and bile secretion were examined using isolated perfused rat liver and rat hepatocyte preparations. ET-1 raised portal pressure dose dependently; administration at a high dose (10(-9) mol) induced a > 200% increase along with reduced bile flow and decreased secretion of bile acid and phospholipids. However, a low dose (10(-10) mol) of ET-1 brought about a < 100% portal pressure rise, enhanced both bile flow and excretion of bile acid and phospholipids, and significantly increased transfer of preadministered horseradish peroxidase (HRP) into bile. In addition, values for Ca2+ concentrations, examined by indo 1 fluorescence, were elevated in isolated hepatocytes after administration of ET-1. Papaverine suppressed the low-dose ET-1 stimulation effects on both portal pressure and bile secretion. Moreover, it also reduced the HRP excretion and suppressed intracellular Ca2+ release. This study demonstrated that ET-1 stimulates vesicular transport, probably via promotion of intracellular Ca2+ release, and, as a result, increases bile acid-dependent bile flow.

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Effects of amino acids on bile acid-dependent and independent bile flow in the isolated perfused rat liver

Journal of Hepatology ◽

10.1016/s0168-8278(99)80138-x ◽

1999 ◽

Vol 30 (5) ◽

pp. 843-849 ◽

Cited By ~ 4

Author(s):

Jean-Pascal De Bandt ◽

Elisabeth Lasnier ◽

Colette Rey ◽

Colette Coudray-Lucas ◽

Raoul Poupon ◽

...

Keyword(s):

Amino Acids ◽

Bile Acid ◽

Rat Liver ◽

Bile Flow ◽

Isolated Perfused Rat Liver ◽

Perfused Rat Liver

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Nifedipine modulation of biliary GSH and GSSG/ conjugate efflux in normal and regenerating rat liver

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.2001.281.1.g85 ◽

2001 ◽

Vol 281 (1) ◽

pp. G85-G94 ◽

Cited By ~ 20

Author(s):

Bo Yang ◽

Ceredwyn E. Hill

Keyword(s):

Bile Acid ◽

Sodium Nitroprusside ◽

Rat Liver ◽

Driving Force ◽

Bile Flow ◽

Organic Anion ◽

High Capacity ◽

Perfused Rat Liver ◽

High Affinity ◽

Glutathione Conjugate Transport

Canalicular glutathione secretion provides the major driving force for bile acid-independent bile flow (BAIF), although the pathways involved are not established. The hypothesis that GSH efflux proceeds by a route functionally distinct from the high-affinity, low-capacity, mrp2-mediated pathway was tested by using perfused rat liver and three choleretic compounds that modify biliary secretion of GSH (the dihydropyridine nifedipine and organic anion probenecid) or GSSG [sodium nitroprusside (SNP)]. Whereas nifedipine (30 μM) stimulated GSH secretion and blocked SNP-stimulated GSSG efflux and choleresis, SNP (1 mM) was ineffective against nifedipine-stimulated GSH efflux or BAIF, suggesting that most GSSG exits through a GSH-inhibitable path independent of high-affinity GSSG/glutathione conjugate transport. Three observations support this proposal. SNP, but not nifedipine, significantly inhibited bromosulfophthalein (BSP, 1 μM) excretion. Probenecid (1 mM) blocked resting or nifedipine-stimulated GSH secretion but only weakly inhibited BSP excretion. Glutathione, but not BSP, efflux capacity was reduced following partial hepatectomy. We suggest GSH efflux is mediated by a high-capacity organic anion pathway capable of GSSG transport when its high-affinity route is saturated.

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