期刊名称：Proceedings of the National Academy of Sciences
印刷版ISSN：0027-8424
电子版ISSN：1091-6490
出版年度：1981
卷号：78
期号：2
页码：986-990
DOI：10.1073/pnas.78.2.986
语种：English
出版社：The National Academy of Sciences of the United States of America
摘要：Transport of sodium, chloride, and taurocholate was studied in primary cultures of adult rat hepatocytes incubated in a balanced electrolyte solution containing 150 mM NaCl, various concentrations of taurocholate, and 22Na, 36Cl, [3H]taurocholate, and 3-O-[3H]methyl-D-glucose. Lithium chloride, choline chloride, or Na2SO4 and mannitol were substituted isotonically for NaCl in selected studies. The steady-state intracellular concentrations of exchangeable sodium and chloride averaged 6.5 mM and 30.1 mM, respectively. Ouabain reversibly increased intracellular sodium concentration. Chloride entry rate was about double that of sodium. Unlike sodium entry, chloride entry rate increased nonlinearly with increasing extracellular concentration. Taurocholate entry exhibited both saturable and nonsaturable components; the former accounting for virtually all taurocholate uptake at concentrations comparable to those found in vivo. Taurocholate was actively concentrated by the cultured cells, with the steady-state intracellular-to-extracellular concentration ratio decreasing from over 50 to about 1 as extracellular taurocholate concentration was increased from 10 {micro}M to 4 mM. Both the saturable uptake component and concentrative taurocholate transport were virtually abolished by substitution of choline or lithium for sodium or by addition of ouabain. Taurocholate entry rate first increased in a sigmoid fashion and then decreased as extracellular sodium concentration was increased from 0 to 150 mM. Sodium entry rate increased in the presence of added taurocholate with an average of one sodium ion accompanying each taurocholate molecule into the cell. These findings indicate that sodium and chloride differ strikingly in their mechanism and rate of entry into cultured rat hepatocytes and in their intracellular concentration. Moreover, hepatocytes concentrate taurocholate by a sodium-coupled mechanism with an apparently equimolar transport stoichiometry.
