Acute reduction of extracellular sodium differentially affects receptor-mediated and K+-induced calcium uptake in PC12 pheochromocytoma cells.
Using a rapid-quench method to measure 45Ca2+ uptake into PC12 cells in suspension, we have studied basal, carbachol-stimulated and K+-induced Ca2+ uptake under control conditions [( Na+]o = 130 mM) and in the presence of acutely lowered extracellular sodium concentration [( Na+]o = 65 mM). Acute reduction of [Na+]o stimulates basal and K+-evoked Ca2+ uptake, but reduces net carbachol-stimulated uptake. Since total Ca2+ uptake measured in the presence of carbachol under control and low [Na+]o conditions is unchanged, the reduction in carbachol-stimulated uptake is due to the increase in basal uptake induced by low [Na+]o. These results reconcile apparently conflicting data regarding a specific Na+ requirement for nicotinic acetylcholine receptor-mediated responses in PC12 cells and adrenal chromaffin cells and suggest a mechanism for loss of nicotinic acetylcholine receptor (nAChR) responsiveness to agonists under low Na+ conditions.
Koski
G
G
Department of Anesthesia, Harvard Medical School, Massachusetts General Hospital, Boston 02114.
Lawrence
K
K
D000818:Animals; D002118:Calcium / Q000493:pharmacokinetics*; D002217:Carbachol / Q000494:pharmacology; D002460:Cell Line; D010673:Pheochromocytoma; D011188:Potassium / Q000494:pharmacology*; D051381:Rats; D012964:Sodium / Q000502:physiology*; D014407:Tumor Cells, Cultured / Q000378:metabolism* / Q000502:physiology
D002217:Carbachol; D012964:Sodium; D011188:Potassium; D002118:Calcium