title: Pertussis toxin pretreatment abolishes dihydropyridine inhibition of calcium flux in the 235-1 pituitary cell line.
abstract: In the present study we used 235-1 cells, a prolactin secreting clone derived from a pituitary tumor. In these cells maitotoxin, a calcium channels activator, likely acting on voltage sensitive calcium channels, increases intracellular free calcium measured by Quin 2 technique. Maitotoxin stimulation of calcium flux was inhibited both by nicardipine and verapamil in a dose dependent manner. Pertussis toxin pretreatment does not modify maitotoxin activation of calcium channels, while completely abolishes nicardipine inhibition of maitotoxin induced voltage sensitive calcium channels activation, without affecting verapamil effect. These results suggest a possible involvement of a pertussis toxin sensitive G protein in dihydropyridine inhibition of voltage sensitive calcium channels.
mesh_terms: D000818:Animals; D002118:Calcium / Q000378:metabolism*; D004095:Dihydropyridines / Q000037:antagonists & inhibitors / Q000494:pharmacology*; D007473:Ion Channels / Q000187:drug effects*; D008387:Marine Toxins / Q000037:antagonists & inhibitors / Q000494:pharmacology; D009529:Nicardipine / Q000037:antagonists & inhibitors / Q000494:pharmacology; D035964:Oxocins; D037342:Pertussis Toxin; D010911:Pituitary Neoplasms / Q000378:metabolism*; D011388:Prolactin / Q000378:metabolism; D014407:Tumor Cells, Cultured; D014700:Verapamil / Q000494:pharmacology; D010566:Virulence Factors, Bordetella / Q000494:pharmacology*; D000095702:Polyether Toxins
chemical_list: D002118:Calcium; D004095:Dihydropyridines; D007473:Ion Channels; D008387:Marine Toxins; D009529:Nicardipine; D035964:Oxocins; D037342:Pertussis Toxin; D011388:Prolactin; D014700:Verapamil; D010566:Virulence Factors, Bordetella; C020394:maitotoxin; D000095702:Polyether Toxins