Nickel: an agent for investigating the relation between hormone-induced Ca2+ influx and bile flow in the perfused rat liver.
Influx of Ca2+ induced by the synergistic action of glucagon plus vasopressin in the perfused rat liver was progressively inhibited by infusing increasing concentrations of Ni2+ to the perfusion medium. The onset of Ca2+ influx following vasopressin administration was delayed and inhibition occurred of both the initial rate of Ca2+ influx as well as the total amount of Ca2+ taken up by the liver. Inhibition of the Ca2+ influx rate was almost maximal at approximately 500 microM Ni2+; half-maximal inhibition occurred at less than 250 microM. Added Ni2+ also delayed the onset of the early transient bile flow peak. In addition, the duration of the transient peak in bile flow was prolonged by approximately 2 min by all concentrations of Ni2+ between 25-500 microM, the greatest amount of bile being released in the presence of 250 microM Ni2+. Concentrations of Ni2+ at 100 microM and above also inhibit the decrease in bile flow to below baseline levels. The data identify a multiple role for Ca2+ mobilisation in bile flow.
Division of Biochemistry and Molecular Biology, Australian National University, Faculty of Science, Canberra, Australia.
A
A
Karjalainen
F L
FL
Bygrave
D000818:Animals; D001646:Bile / Q000378:metabolism*; D002118:Calcium / Q000378:metabolism*; D004357:Drug Synergism; D005934:Glucagon / Q000494:pharmacology*; D017136:Ion Transport / Q000187:drug effects; D008099:Liver / Q000187:drug effects / Q000378:metabolism*; D008297:Male; D009532:Nickel / Q000494:pharmacology*; D010477:Perfusion; D051381:Rats; D017208:Rats, Wistar; D014667:Vasopressins / Q000494:pharmacology*
D014667:Vasopressins; D009532:Nickel; D005934:Glucagon; D002118:Calcium