title: Modification by pertussis toxin of the responses of bovine anterior pituitary cells to acetylcholine and dopamine: effects on hormone secretion and 86Rb efflux.
abstract: Acetylcholine is known to stimulate the secretion of growth hormone and prolactin and the efflux of 86Rb from bovine anterior pituitary cells: dopamine prevents the stimulation of 86Rb efflux and of prolactin but not growth hormone secretion. The sensitivity of these responses to pertussis toxin has been determined. Treatment of bovine anterior pituitary cells in primary culture with pertussis toxin (18 h, 100 ng/ml) did not modify the stimulation of prolactin secretion by acetylcholine, but prevented its inhibition by dopamine. In lactotrophs, dopamine but not acetylcholine receptors are therefore coupled to secretion through a pertussis toxin substrate. The stimulation of 86Rb efflux by acetylcholine was also unaffected by pertussis toxin and, again, its inhibition by dopamine was prevented. Treatment of the cells with pertussis toxin enhanced the secretion of growth hormone in response to acetylcholine. Nitrendepine (1 mumol/l) prevented the cholinergic stimulation of growth hormone but not prolactin secretion from these cells. Acetylcholine increased the cytoplasmic calcium concentration and this rise was enhanced by treatment of the cells with pertussis toxin. Nitrendepine partially inhibited the rise in calcium caused by acetylcholine, and prevented the enhancement of the rise following pertussis toxin treatment. Cholinergic stimulation of growth hormone therefore depends on calcium entry through nitrendepine-sensitive channels, whereas stimulation of prolactin secretion does not, and in somatotrophs a pertussis toxin substrate may limit calcium entry through these channels. These different sensitivities of somatotrophs and lactotrophs to pertussis toxin and nitrendepine may reflect differences in the properties of the predominant calcium currents in the two cell types.
authors.affiliation: Department of Biochemistry, Medical School, University of Bristol.
authors.forename: J G
authors.initials: JG
authors.lastname: Schofield
authors.forename: A I
authors.initials: AI
authors.lastname: Khan
authors.forename: A
authors.initials: A
authors.lastname: Wood
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology*; D000818:Animals; D002118:Calcium / Q000378:metabolism; D002417:Cattle; D002478:Cells, Cultured; D004298:Dopamine / Q000494:pharmacology*; D004347:Drug Interactions; D005260:Female; D013006:Growth Hormone / Q000378:metabolism; D009568:Nitrendipine / Q000494:pharmacology; D037342:Pertussis Toxin; D010903:Pituitary Gland, Anterior / Q000187:drug effects* / Q000378:metabolism; D010907:Pituitary Hormones / Q000378:metabolism*; D011188:Potassium / Q000378:metabolism; D011388:Prolactin / Q000378:metabolism; D012414:Rubidium Radioisotopes; D010566:Virulence Factors, Bordetella / Q000494:pharmacology*
chemical_list: D010907:Pituitary Hormones; D012414:Rubidium Radioisotopes; D010566:Virulence Factors, Bordetella; D011388:Prolactin; D013006:Growth Hormone; D009568:Nitrendipine; D037342:Pertussis Toxin; D000109:Acetylcholine; D011188:Potassium; D002118:Calcium; D004298:Dopamine