Mobilization of cellular calcium-45 and lead-210: effect of physiological stimuli.
Isolated rat hepatocytes in primary culture were used as a model system to evaluate the effects of selected hormones and culture conditions on the efflux of calcium-45 and lead-210 from cells labeled with these isotopes. Alpha-adrenergic stimuli, angiotensin, vasopressin, dibutyryl adenosine 3',5'-monophosphate, and reduced phosphate concentrations in the medium increased the efflux of calcium-45 and lead-210. Glucagon and insulin had no effect, but increased phosphate concentrations decreased the efflux of both isotopes. Experiments with hepatocytes cultured in a medium free of calcium and lead demonstrated that the increased efflux of calcium-45 and lead-210 induced by hormones was the result of mobilization of the ions from intracellular stores. The data indicate that the physiological stimuli that mobilized calcium ions also mobilized lead ions, and that the mobilized lead would be available to interact with calcium-mediated cell functions.
D000804:Angiotensin II / Q000494:pharmacology; D000818:Animals; D003994:Bucladesine / Q000494:pharmacology; D002132:Calcium Radioisotopes / Q000378:metabolism*; D002478:Cells, Cultured; D004837:Epinephrine / Q000494:pharmacology; D007328:Insulin / Q000494:pharmacology; D007854:Lead / Q000378:metabolism*; D008099:Liver / Q000166:cytology; D010710:Phosphates / Q000494:pharmacology; D011433:Propranolol / Q000494:pharmacology; D011868:Radioisotopes; D051381:Rats; D014667:Vasopressins / Q000494:pharmacology
D002132:Calcium Radioisotopes; D007328:Insulin; D010710:Phosphates; D011868:Radioisotopes; D014667:Vasopressins; D000804:Angiotensin II; D007854:Lead; D003994:Bucladesine; D011433:Propranolol; D004837:Epinephrine