Na-Pi cotransport in LLC-PK1 cells: fast adaptive response to Pi deprivation.
A short-term regulation of the Na-dependent transport of Pi in LLC-PK1 cells by the extracellular concentration of Pi is described. Pi deprivation of the cells for 10 min led to an increase (30%) of the Na-Pi cotransport activity, whereas the Na-dependent D-glucose transport system was not affected. This regulatory phenomenon was not affected by the presence of cycloheximide. The same adaptive response was observed in apical membrane vesicles isolated from rapidly adapted cells. In the isolated membranes, increased Na-Pi cotransport is characterized by an increase of the maximal rate of uptake (control: 193 +/- 15; adapted: 306 +/- 51 pmol X mg-1 X 15 s-1), whereas the apparent Km for Pi remained constant. The results suggest that LLC-PK1 cells possess a mechanism or mechanisms that allow a rapid "activation" and "inactivation" of Na-dependent Pi transport systems as a function of the concentration of the extracellular Pi.
D000222:Adaptation, Physiological / Q000187:drug effects; D000818:Animals; D001692:Biological Transport; D002460:Cell Line; D003513:Cycloheximide / Q000494:pharmacology; D007668:Kidney / Q000166:cytology / Q000378:metabolism*; D007700:Kinetics; D008715:Methionine / Q000378:metabolism; D009994:Osmolar Concentration; D010710:Phosphates / Q000172:deficiency / Q000378:metabolism*; D012964:Sodium / Q000378:metabolism*; D013552:Swine; D013997:Time Factors
D010710:Phosphates; D003513:Cycloheximide; D012964:Sodium; D008715:Methionine