Ca(2+) influx stimulated phospholipase C activity in bovine adrenal chromaffin cells: responses to K(+) depolarization and histamine

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 an...

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Veröffentlicht in:European journal of pharmacology 2000-06, Vol.398 (2), p.199
Hauptverfasser: Roberts-Thomson, E L, Saunders, H I, Palmer, S M, Powis, D A, Dunkley, P R, Bunn, S J
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container_issue 2
container_start_page 199
container_title European journal of pharmacology
container_volume 398
creator Roberts-Thomson, E L
Saunders, H I
Palmer, S M
Powis, D A
Dunkley, P R
Bunn, S J
description 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.
doi_str_mv 10.1016/S0014-2999(00)00201-6
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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.</abstract><cop>Netherlands</cop><pmid>10854831</pmid><doi>10.1016/S0014-2999(00)00201-6</doi></addata></record>
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subjects Adrenal Glands - cytology
Adrenal Glands - drug effects
Adrenal Glands - metabolism
Animals
Calcium - metabolism
Calcium Channel Blockers - pharmacology
Calcium Channels - drug effects
Calcium Channels - physiology
Calcium Signaling - drug effects
Cattle
Cells, Cultured
Chromaffin Cells - cytology
Chromaffin Cells - drug effects
Chromaffin Cells - metabolism
Histamine - pharmacology
Imidazoles - pharmacology
Inositol Phosphates - metabolism
Nifedipine - pharmacology
omega-Conotoxin GVIA - pharmacology
omega-Conotoxins - pharmacology
Potassium - pharmacology
Type C Phospholipases - drug effects
Type C Phospholipases - metabolism
title Ca(2+) influx stimulated phospholipase C activity in bovine adrenal chromaffin cells: responses to K(+) depolarization and histamine
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