title: Ca(2+) influx stimulated phospholipase C activity in bovine adrenal chromaffin cells: responses to K(+) depolarization and histamine.
abstract: The role of Ca(2+) influx in activating phospholipase C in bovine adrenal chromaffin cells has been investigated. Phospholipase C activity in response to K(+) depolarization (56 mM) was blocked by the L-type Ca(2+) channel antagonist nifedipine and partially inhibited by the omega-conotoxins GVIA and MVIIC. In contrast, phospholipase C activity in response to histamine receptor activation was unaffected by omega-conotoxin GVIA and partially inhibited by omega-conotoxin MVIIC or nifedipine. This response was however markedly inhibited by the non-selective Ca(2+) channel antagonists La(3+) or 1-[beta-[3-(4-Methoxyphenyl)propoxy]-4-methoyphenethyl]-H-imidazol e (SKF-96365). Despite this Ca(2+) dependence phospholipase C activity was not increased during periods of "capacitative" Ca(2+) inflow generated by histamine-, caffeine- or thapsigargin-mediated depletion of internal Ca(2+) stores. Thus, while Ca(2+) influx in response to K(+) depolarization or G-protein receptor activation can increase phospholipase C activity in these cells, in the latter case it appears to be ineffective unless there is concurrent agonist occupation of the receptor.
authors.affiliation: The Neuroscience Group, Faculty of Medicine and Health Sciences, University of Newcastle, Callaghan, New South Wales, Newcastle, Australia.
authors.forename: E L
authors.initials: EL
authors.lastname: Roberts-Thomson
authors.forename: H I
authors.initials: HI
authors.lastname: Saunders
authors.forename: S M
authors.initials: SM
authors.lastname: Palmer
authors.forename: D A
authors.initials: DA
authors.lastname: Powis
authors.forename: P R
authors.initials: PR
authors.lastname: Dunkley
authors.forename: S J
authors.initials: SJ
authors.lastname: Bunn
mesh_terms: D000311:Adrenal Glands / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D000818:Animals; D002118:Calcium / Q000378:metabolism*; D002121:Calcium Channel Blockers / Q000494:pharmacology; D015220:Calcium Channels / Q000187:drug effects / Q000502:physiology; D020013:Calcium Signaling / Q000187:drug effects; D002417:Cattle; D002478:Cells, Cultured; D019439:Chromaffin Cells / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D006632:Histamine / Q000494:pharmacology; D007093:Imidazoles / Q000494:pharmacology; D007295:Inositol Phosphates / Q000378:metabolism; D009543:Nifedipine / Q000494:pharmacology; D011188:Potassium / Q000494:pharmacology; D010738:Type C Phospholipases / Q000187:drug effects / Q000378:metabolism*; D020866:omega-Conotoxin GVIA / Q000494:pharmacology; D020960:omega-Conotoxins / Q000494:pharmacology
chemical_list: D002121:Calcium Channel Blockers; D015220:Calcium Channels; D007093:Imidazoles; D007295:Inositol Phosphates; D020960:omega-Conotoxins; C075851:omega-conotoxin-MVIIC; D006632:Histamine; D020866:omega-Conotoxin GVIA; D010738:Type C Phospholipases; C063159:1-(2-(3-(4-methoxyphenyl)propoxy)-4-methoxyphenylethyl)-1H-imidazole; D009543:Nifedipine; D011188:Potassium; D002118:Calcium