Iodipamide uptake by rat liver plasma membrane vesicles enriched in the sinusoidal fraction: evidence for a carrier-mediated transport dependent on membrane potential

1986 ◽  
Vol 855 (1) ◽  
pp. 157-168 ◽  
Author(s):  
M. Täfler ◽  
K. Ziegler ◽  
M. Frimmer
1992 ◽  
Vol 263 (3) ◽  
pp. G338-G344 ◽  
Author(s):  
A. M. Torres ◽  
J. V. Rodriguez ◽  
G. C. Lunazzi ◽  
C. Tiribelli

To investigate the molecular requirements and mechanisms for the hepatic uptake of phthaleins, the transport of tetrabromosulfonephthalein (TBS) was investigated in basolateral rat liver plasma membrane vesicles. TBS uptake was electrogenic as greatly accelerated by the creation of a positive-inside membrane potential by the addition of valinomycin in the presence of an inwardly directed potassium gradient. No effect was observed when the ionophore was added in the presence of a sodium gradient. The transport occurred into an osmotic-sensitive space and was saturable with an apparent Michaelis constant of 5.32 +/- 0.56 microM and a maximal velocity of 9.23 +/- 0.25 nmol.s-1.mg protein-1 (mean +/- SD, n = 3 experiments). TBS uptake was directly related to the extra-vesicular pH, indicating the deprotonated quinoid negative-charged form of the dye as the transported species. In contrast, TBS uptake was inversely related to the intravesicular pH, suggesting that protonation inside the vesicles may act as an efficient trap in transport process. Addition of polyclonal monospecific anti-bilitranslocase antibody to liver vesicles specifically inhibited TBS uptake rate (3.27 +/- 0.17 vs. 5.82 +/- 0.61 nmol.s-1.mg protein-1, n = 3, P less than 0.001). These data indicate that TBS is electrogenically transported across the liver cell plasma membrane by bilitranslocase. They also indicate that the presence of a negative charged group on the benzenic ring of the ligand is important in accounting for the transport.


1992 ◽  
Vol 103 (3) ◽  
pp. 1056-1065 ◽  
Author(s):  
Richard H. Moseley ◽  
Pankaj G. Vashi ◽  
Suzanne M. Jarose ◽  
Chris J. Dickinson ◽  
Patricia A. Permoad

1985 ◽  
Vol 75 (4) ◽  
pp. 1256-1263 ◽  
Author(s):  
P J Meier ◽  
R Knickelbein ◽  
R H Moseley ◽  
J W Dobbins ◽  
J L Boyer

1986 ◽  
Vol 251 (5) ◽  
pp. G656-G664 ◽  
Author(s):  
G. Hugentobler ◽  
P. J. Meier

The mechanisms and driving forces for hepatic uptake of sulfate were investigated in basolateral (sinusoidal) rat liver plasma membrane vesicles. A transmembrane pH difference (pH 8.0 inside, 6.0 outside) stimulated sulfate uptake above equilibrium (“overshoot”). This pH gradient-stimulated sulfate uptake was saturable with increasing concentrations of sulfate and could be inhibited by probenecid, 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS), carbonyl cyanide p-(trifluoromethoxy)-phenylhydrazone, and nigericin. At low buffer concentrations and pH 6.0 an inwardly directed sodium gradient also stimulated sulfate uptake. This sodium-dependent sulfate uptake could be inhibited by amiloride and DIDS, indicating indirect coupling of sodium and sulfate flux through concomitant sodium-proton and sulfate-hydroxyl exchange. Cisinhibition of initial pH gradient-stimulated sulfate uptake, as well as transstimulation of sulfate uptake under pH-equilibrated conditions (pH 7.5 inside and outside), were observed with sulfate, thiosulfate, oxalate, and succinate, but not with chloride, bicarbonate, acetate, lactate, pyruvate, p-aminohippurate, citrate, glutamate, aspartate, and taurocholate. Furthermore, cholate and sulfobromophthalein exhibited competitive inhibition of pH gradient-stimulated sulfate uptake. In addition, an inside-to-outside hydroxyl gradient also stimulated uptake of cholate and this pH gradient-sensitive portion of cholate uptake was inhibited by extravesicular sulfate. In contrast to basolateral membranes, no evidence for multispecific sulfate-hydroxyl exchange was found in canalicular plasma membrane vesicles.


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