scholarly journals Ion selectivity and gating of small conductance Ca(2+)-activated K+ channels in cultured rat adrenal chromaffin cells.

1994 ◽  
Vol 481 (3) ◽  
pp. 555-570 ◽  
Author(s):  
Y B Park
Keyword(s):  
Chromaffin Cells ◽  
Ion Selectivity ◽  
Adrenal Chromaffin Cells ◽  
K Channels ◽  
Adrenal Chromaffin ◽  
Small Conductance

scholarly journals Hypoxia-Induced Catecholamine Release and Intracellular Ca2+ Increase via Suppression of K+ Channels in Cultured Rat Adrenal Chromaffin Cells

2002 ◽  
Vol 69 (1) ◽  
pp. 377-387 ◽  
Author(s):  
Noriko Mochizuki-Oda ◽  
Yuko Takeuchi ◽  
Kiyoshi Matsumura ◽  
Yoshio Oosawa ◽  
Yasuyoshi Watanabe
Keyword(s):  
Chromaffin Cells ◽  
Catecholamine Release ◽  
Adrenal Chromaffin Cells ◽  
K Channels ◽  
Adrenal Chromaffin

Nitric oxide activates Ca2+-activated K+ channels in cultured bovine adrenal chromaffin cells

1998 ◽  
Vol 248 (2) ◽  
pp. 127-129 ◽  
Author(s):  
Chun-He Chen ◽  
Hitoshi Houchi ◽  
Masahar Ohnaka ◽  
Sadaichi Sakamoto ◽  
Yasuharu Niwa ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Chromaffin Cells ◽  
Adrenal Chromaffin Cells ◽  
K Channels ◽  
Adrenal Chromaffin

Hypoxia-sensitive K+ channels in rat adrenal chromaffin cells

1998 ◽  
Vol 31 ◽  
pp. S354
Author(s):  
Noriko Oda-Mochizuki ◽  
Yuko Takeuchi ◽  
Yoshio Oosawa ◽  
Yasuyoshi Watanabe
Keyword(s):  
Chromaffin Cells ◽  
Adrenal Chromaffin Cells ◽  
K Channels ◽  
Adrenal Chromaffin

Modulation by L-type Ca2+ channels and apamin-sensitive K+ channels of muscarinic responses in cat chromaffin cells

1994 ◽  
Vol 266 (5) ◽  
pp. C1432-C1439 ◽  
Author(s):  
G. Uceda ◽  
A. R. Artalejo ◽  
M. T. de la Fuente ◽  
M. G. Lopez ◽  
A. Albillos ◽  
...  
Keyword(s):  
Chromaffin Cells ◽  
Channel Blocker ◽  
Muscarinic Agonist ◽  
Adrenal Chromaffin Cells ◽  
Tonic Component ◽  
K Channels ◽  
Biphasic Pattern ◽  
Phasic Component ◽  
Adrenal Chromaffin ◽  
Ca2 Channels

In the perfused cat adrenal gland stimulated with the muscarinic agonist methacholine chloride (100 microM for 3 min), two components were detected in the catecholamine secretory response: 1) an early phasic component that peaked at 300 ng/5 s catecholamine release and 2) a tonic component whose peak was transient and declined to a plateau of about 140 ng/5 s. Apamin (0.1 microM) increased the phasic component to 1,200 ng/5 s and the tonic component to approximately 350 ng/5 s. In single fura 2-loaded cat adrenal chromaffin cells, the cytosolic Ca2+ concentration ([Ca2+]i) also followed a biphasic pattern after stimulation with methacholine. Depletion of extracellular Ca2+ reduced the phasic [Ca2+]i peak by > 50% and the phasic secretory peak by approximately 90%; both the tonic components of [Ca2+]i and secretion were abolished. Depletion of intracellular Ca2+ pools decreased the phasic and tonic components of [Ca2+]i and secretion with respect to control values; however, the phasic components diminished more than the tonic components of [Ca2+]i and secretion. Although 3 microM furnidipine (a dihydropyridine L-type Ca2+ channel blocker) inhibited the phasic component of [Ca2+]i and secretion, its effects were more pronounced on the tonic component. omega-Conotoxin GVIA (1 microM, an N-type Ca2+ channel blocker) did not affect the [Ca2+]i or the methacholine secretory responses. The secretion peak seems to depend on both extracellular free Ca2+ (Cao2+) entry through L-type Ca2+ channels as well as on the mobilization of Ca2+ from intracellular stores; the plateau depends only on Cao2+ entry through L-type Ca2+ channels.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Oxygen sensitivity in the sheep adrenal medulla: role of SK channels

2001 ◽  
Vol 281 (5) ◽  
pp. C1434-C1441 ◽  
Author(s):  
Damien J. Keating ◽  
Grigori Y. Rychkov ◽  
Michael L. Roberts
Keyword(s):  
Adrenal Medulla ◽  
Chromaffin Cells ◽  
Catecholamine Secretion ◽  
Resting Potential ◽  
Sk Channels ◽  
Adrenal Chromaffin Cells ◽  
Simultaneous Application ◽  
Adrenal Chromaffin ◽  
Small Conductance

The hypoxia-evoked secretion of catecholamines from the noninnervated fetal adrenal gland is essential for surviving intrauterine hypoxemia. The ion channels responsible for the initial depolarization that leads to catecholamine secretion have not been identified. Patch-clamp studies of adrenal chromaffin cells isolated from fetal and adult sheep revealed the presence of a Ca2+-dependent K+ current that was reduced by hypoxia. Apamin, a blocker of small-conductance K+ (SK) channels, reduced the Ca2+-dependent K+current, and the sensitivity of the channels to apamin indicated that the channels involved were of the SK2 subtype. In the presence of apamin, the hypoxia-evoked change in K+ currents was largely eliminated. Both hypoxia and apamin blocked a K+current responsible for maintaining the resting potential of the cell, and the depolarization resulting from both led to an influx of Ca2+. Simultaneous application of hypoxia and apamin did not potentiate the increase in cytosolic Ca2+ concentration beyond that seen with either agent alone. Similar results were seen with curare, another blocker of SK channels. These results indicate that closure of SK2 channels would be the initiating event in the hypoxia-evoked catecholamine secretion in the adrenal medulla.

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