Lipid mediators on the extracellular Ca^<2+>-sensing in parathyroid cells

点击翻译按钮获取中文摘要

Parathyroid cells directly monitor extracellular Ca^<2+> concentration using Ca receptors(CaR). In isolated frog parathyroid cells, high extracellular Ca^<2+> concentration induces a large increase in chloride conductance. In the present study, we investigated how extracellular Ca^<2+> increases parathyroid chloride conductance while recording the whole cell current. The parathyroid cells displayed a TTX-sensitive Na^+ current in response to the depolarizing voltage steps from a holding potential of -84 mV. Extracellular Win55,212-2 greatly inhibited the voltage-gated Na+ current, suggesting that the activity can be modified by the cannabinoids. High extracellular Ca^<2+> induced an increase of the inward current at -50 mV in a dose-dependent manner. The apparent EC_<50>for Ca^<2+>was about 6 mM. When either U73122(an inhibitor of PLC), tetrahydrolipstatin(an inhibitor of DAG lipase), or methyl arachidonyl fluorophosphonate(MAFP, an inhibitor of MAG lipase)was applied extracellularly, the magnitude of extracellular Ca^<2+>-induced current decreased significantly. Internal dialysis of 2-arachidonyl glycerol(2-AG)induced a Gd^<3+>-sensitive inward current, but internal 2-AG ether did not elicit any response. Internal dialysis of arachidonic acid also induced Gd^<3+>-sensitive inward current. The results suggest that the arachidonic acid metabolite is involved in the extracellular Ca^<2+>-sensing of frog parathyroid cells.