TY - JOUR
T1 - Stimulus-secretion coupling in porcine adrenal chromaffin cells
T2 - Effect of dexamethasone
AU - Fuller, Lynn Z.
AU - Lu, Chengbiao
AU - McMahon, Douglas G.
AU - Lindemann, Merlin D.
AU - Jorgensen, Mark S.
AU - Rau, Shane W.
AU - Sisken, Jesse E.
AU - Jackson, Brian A.
PY - 1997/8/15
Y1 - 1997/8/15
N2 - Recent studies from this laboratory established that dexamethasone (DEX) potentiates Ca2+ current via voltage-gated Ca2+ channels (VGCC), and as a consequence potentiates agonist-induced cytosolic Ca2+ transients in rat adrenal chromaffin cells. The present study examined whether DEX can also modulate VGCC activity and agonist-induced cytosolic Ca2+ transients in porcine adrenal medullary chromaffin (PAMC) cells, and if so whether this results in alterations in catecholamine secretion. Forty-eight-hr exposure to 1 μM DEX significantly increased peak Ca2+ current (Δ + 138%; n = 6; P < 0.05) in PAMC cells. DEX treatment also significantly potentiated the increase in cytosolic Ca2+ in response to membrane depolarization with KCl (Δ + 20%; n = 29; P < 0.05), but did not affect the amplitude of Ca2+ transients elicited by nicotine or acetylcholine. Despite the potentiation of intracellular Ca2+, DEX treatment had no effect on KCl-induced secretion of either norepinephrine or epinephrine. These data demonstrate that as in the rat chromafin cell, DEX can also increase VGCC activity in PAMC cells. However, the subsequent potentiation of selected agonist-induced increases in intracellular Ca2+ does not appear to be sufficient to alter catecholamine secretion.
AB - Recent studies from this laboratory established that dexamethasone (DEX) potentiates Ca2+ current via voltage-gated Ca2+ channels (VGCC), and as a consequence potentiates agonist-induced cytosolic Ca2+ transients in rat adrenal chromaffin cells. The present study examined whether DEX can also modulate VGCC activity and agonist-induced cytosolic Ca2+ transients in porcine adrenal medullary chromaffin (PAMC) cells, and if so whether this results in alterations in catecholamine secretion. Forty-eight-hr exposure to 1 μM DEX significantly increased peak Ca2+ current (Δ + 138%; n = 6; P < 0.05) in PAMC cells. DEX treatment also significantly potentiated the increase in cytosolic Ca2+ in response to membrane depolarization with KCl (Δ + 20%; n = 29; P < 0.05), but did not affect the amplitude of Ca2+ transients elicited by nicotine or acetylcholine. Despite the potentiation of intracellular Ca2+, DEX treatment had no effect on KCl-induced secretion of either norepinephrine or epinephrine. These data demonstrate that as in the rat chromafin cell, DEX can also increase VGCC activity in PAMC cells. However, the subsequent potentiation of selected agonist-induced increases in intracellular Ca2+ does not appear to be sufficient to alter catecholamine secretion.
KW - Adrenal medulla
KW - Catecholamines
KW - Chromaffin cell
KW - Fura-2
KW - Glucocorticoids
KW - Intracellular calcium
KW - Voltage-gated calcium channels
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U2 - 10.1002/(SICI)1097-4547(19970815)49:4<416::AID-JNR3>3.0.CO;2-B
DO - 10.1002/(SICI)1097-4547(19970815)49:4<416::AID-JNR3>3.0.CO;2-B
M3 - Article
C2 - 9285518
AN - SCOPUS:0030814136
VL - 49
SP - 416
EP - 424
IS - 4
ER -