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  • 1
    ISSN: 1432-1424
    Keywords: taurine ; sodium-coupled transport ; Na+, K+-ATPase ; retinal pigment epithelium ; retina
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Summary The apical surface of the retinal pigment epithelium (RPE) faces the neural retina whereas its basal surface faces the choroid. Taurine, which is necessary for normal vision, is released from the retina following light exposure and is actively transported from retina to choroid by the RPE. In these experiments, we have studied the effects of taurine on the electrical properties of the isolated RPE of the bullfrog, with a particular focus on the effects of taurine on the apical Na+−K+ pump. Acute exposure of the apical, but not basal, membrane of the RPE to taurine decreased the normally apical positive transepithelial potential (TEP). This TEP decrease was generated by a depolarization of the RPE apical membrane and did not occur when the apical bath contained sodium-free medium. With continued taurine exposure, the initial TEP decrease was sometimes followed by a recovery of the TEP toward baseline. This recovery was abolished by strophanthidin or ouabain, indicating involvement of the apical Na+−K+ pump. To further explore the effects of taurine on the Na+−K+ pump, barium was used to block apical K+ conductance and unmask a stimulation of the pump that is produced by increasing apical [K+] 0 . Under these conditions, increasing [K+] 0 hyperpolarized the apical membrane and increased TEP. Taurine reversibly doubled these responses, but did not change total epithelial resistance or the ratio of apical-to-basal membrane resistance, and ouabain abolished these responses. Collectively, these findings indicate the presence of an electrogenic Na+/taurine cotransport mechanism in the apical membrane of the bullfrog RPE. They also provide direct evidence that taurine produces a sodium-dependent increase in electrogenic pumping by the apical Na+−K+ pump.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-1424
    Keywords: Na+/HCO 3 − cotransport ; symport ; microelectrodes ; membrane potential ; SBFI ; ion transport
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Summary Recent studies in hepatocytes indicate that Na+-coupled HCO 3 − transport contributes importantly, to regulation of intracellular pH and membrane HCO 3 − transport. However, the direction of net coupled Na+ and HCO 3 − movement and the effect of HCO 3 − on Na+ turnover and Na+/K+ pump activity are not known. In these studies, the effect of HCO 3 − on Na+ influx and turnover were measured in primary rat hepatocyte cultures with22Na+, and [Na+] i was measured in single hepatocytes using the Na+-sensitive fluorochrome SBFI. Na+/K+ pump activity was measured in intact perfused rat liver and hepatocyte monolayers as Na+-dependent or ouabain-suppressible86Rb uptake, and was measured in single hepatocytes as the effect of transient pump inhibition by removal of extracellular K+ on membrane potential difference (PD) and [Na+] i . In hepatocyte monolayers, HCO 3 − increased22Na+ entry and turnover rates by 50–65%, without measurably altering22Na+ pool size or cell volume, and HCO 3 − also increased Na+/K+ pump activity by 70%. In single cells, exposure to HCO 3 − produced an abrupt and sustained rise in [Na+] i , from ≈8 to 12mm. Na+/K+ pump activity assessed in single cells by PD excursions during transient K+ removal increased ≃2.5-fold in the presence of HCO 3 − , and the rise in [Na+] i produced by inhibition of the Na+/K+ pump was similarly increased ≃2.5-fold in the presence of HCO 3 − . In intact perfused rat liver, HCO 3 − increased both Na+/K+ pump activity and O2 consumption. These findings indicate that, in hepatocytes, net coupled Na+ and HCO 3 − movement is inward and represents a major determinant of Na+ influx and Na+/K+ pump activity. About half of hepatic Na+/K+ pump activity appears dedicated to recycling Na+ entering in conjunction with HCO 3 − to maintain [Na+] i within the physiologic range.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Digestive diseases and sciences 34 (1989), S. S5 
    ISSN: 1573-2568
    Keywords: bile acid ; ursodeoxycholic acid ; intracellular pH, membrane transport ; biotransformation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract This review focuses on mechanisms of bile acid transport across the basolateral and canalicular hepatocyte plasma membranes and on ursodeoxycholic acid (UDCA) hypercholeresis and biotransformation. Conjugated trihydroxy bile acids enter hepatocytes via a sodium-coupled mechanism localized to the basolateral membrane, which is saturable, concentrative, inhibited by other bile acids as well as by furosemide and bumetanide, and exhibits developmental changes in rats and probably also in humans. The stoichiometry of sodium-coupled bile acid uptake has been controversial. Hydrophobic, unconjugated dihydroxy and monohydroxy bile acids, including UDCA, enter hepatocytes more rapidly than does taurocholate, and their uptake is largely nonsaturable and sodium independent. A hydroxyl-exchange mechanism that mediates the uptake of cholic acid has also been reported, but its existence is controversial. Current evidence suggests that a 49-kDa protein mediates Na+-dependent taurocholate uptake and that a 54-kDa protein is involved in Na+-independent bile acid uptake. Studies with canalicular membrane vesicles have demonstrated saturable, sodium-independent taurocholate transport, which is sensitive to electrical potential, exhibits trans-stimulation, and appears to be mediated by a 100-kDa canalicular membrane glycoprotein. Studies in mutant rats with conjugated hyperbilirubinemia suggest the presence of a separate canalicular transport mechanism utilized by sulfated bile acids and organic anions such as bilirubin and sulfobromophthalein. UDCA produces in some species a dramatic hypercholeresis that is greater than expected based on the osmotic effect of the secreted bile acid. The hypercholeresis appears attributable to stimulation of biliary bicarbonate output and is decreased or abolished in the perfused rat liver by amiloride or perfusate Na+ substitution. These same maneuvers dramatically alter UDCA biotransformation (unconjugated UDCA disappears from bile, and UDCA glucuronide becomes a major metabolite) and lower hepatocyte intracellular pH. These and other findings indicate that UDCA hypercholeresis is tightly linked to biliary excretion of the unconjugated species and suggest that UDCA biotransformation may be influenced by intracellular pH.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Digestive diseases and sciences 23 (1978), S. S9 
    ISSN: 1573-2568
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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