J Physiol Wellcome Trust-funded researchers
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

J Physiol Volume 512, Number 2, 421-434, October 15, 1998
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Thompson, R. J.
Right arrow Articles by Nurse, C. A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Thompson, R. J.
Right arrow Articles by Nurse, C. A.
The Journal of Physiology (1998), 512.2, pp. 421-434
© Copyright 1998 The Physiological Society

Anoxia differentially modulates multiple K+ currents and depolarizes neonatal rat adrenal chromaffin cells

Roger J. Thompson and Colin A. Nurse

Department of Biology, McMaster University, Hamilton, Ontario, Canada L8S 4K1

  1. Using perforated-patch, whole cell recording, we investigated the membrane mechanisms underlying O2 chemosensitivity in neonatal rat adrenomedullary chromaffin cells (AMC) bathed in extracellular solution containing tetrodotoxin (TTX; 0·5-1 µM), with or without blockers of calcium entry.

  2. Under voltage clamp, low PO2 (0-15 mmHg) caused a graded and reversible suppression in macroscopic outward K+ current. The suppression during anoxia (POµ = 0 mmHg) was ~35 % (voltage step from -60 to +30 mV) and was due to a combination of several factors: (i) suppression of a cadmium-sensitive, Ca2+-dependent K+ current, IK(CaO2); (ii) suppression of a Ca2+-insensitive, delayed rectifier type K+ current, IK(VO2); (iii) activation of a glibenclamide- (and Ca2+)-sensitive current, IK(ATP).

  3. During normoxia (PO2 = 150 mmHg), application of pinacidil (100 µM), an ATP-sensitive potassium channel (KATP) activator, increased outward current density by 45·0 ± 7·0 pA pF-1 (step from -60 to + 30 mV), whereas the KATP blocker glibenclamide (50 µM) caused only a small suppression by 6·3 ± 4·0 pA pF-1. In contrast, during anoxia the presence of glibenclamide resulted in a substantial reduction in outward current density by 24·9 ± 7·9 pA pF-1, which far exceeded that seen in its absence. Thus, activation of IK(ATP) by anoxia appears to reduce the overall K+ current suppression attributable to the combined effects of IK(CaO2) and IK(VO2).

  4. Pharmacological tests revealed that IK(CaO2) was carried predominantly by maxi-K+ or BK potassium channels, sensitive to 50-100 nM iberiotoxin; this current also accounted for the major portion (~60 %) of the anoxic suppression of outward current. Tetraethylammonium (TEA; 10-20 mM) blocked all of the anoxia-sensitive K+ currents recorded under voltage clamp, i.e. IK(CaO2), IK(VO2) and IK(ATP).

  5. Under current clamp, anoxia depolarized neonatal AMC by 10-15 mV from a resting potential of ~-55 mV. At least part of this depolarization persisted in the presence of either TEA, Cd2+, 4-aminopyridine or charybdotoxin, suggesting the presence of anoxia-sensitive mechanisms additionalto those revealed under voltage clamp. In Na+/Ca2+-free solutions, the membrane hyperpolarized, though at least a portion of the anoxia-induced depolarization persisted.

  6. In the presence of glibenclamide, the anoxia-induced depolarization increased significantly to ~25 mV, suggesting that activation of KATP channels may function to attenuate the anoxia-induced depolarization or receptor potential.



This article has been cited by other articles:


Home page
 FASEB J.Home page
J. Buttigieg, S. Brown, M. Zhang, M. Lowe, A. C. Holloway, and C. A. Nurse
Chronic nicotine in utero selectively suppresses hypoxic sensitivity in neonatal rat adrenal chromaffin cells
FASEB J, May 1, 2008; 22(5): 1317 - 1326.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Cell Physiol.Home page
J. Buttigieg, S. T. Brown, M. Lowe, M. Zhang, and C. A. Nurse
Functional mitochondria are required for O2 but not CO2 sensing in immortalized adrenomedullary chromaffin cells
Am J Physiol Cell Physiol, April 1, 2008; 294(4): C945 - C956.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
A. M. Evans, K. J. W. Mustard, C. N. Wyatt, C. Peers, M. Dipp, P. Kumar, N. P. Kinnear, and D. G. Hardie
Does AMP-activated Protein Kinase Couple Inhibition of Mitochondrial Oxidative Phosphorylation by Hypoxia to Calcium Signaling in O2-sensing Cells?
J. Biol. Chem., December 16, 2005; 280(50): 41504 - 41511.
[Abstract] [Full Text] [PDF]

Home page
 J. Neurosci.Home page
A. M. Munoz-Cabello, J. J. Toledo-Aral, J. Lopez-Barneo, and M. Echevarria
Rat Adrenal Chromaffin Cells Are Neonatal CO2 Sensors
J. Neurosci., July 13, 2005; 25(28): 6631 - 6640.
[Abstract] [Full Text] [PDF]

Home page
 ScienceHome page
S. E. J. Williams, P. Wootton, H. S. Mason, J. Bould, D. E. Iles, D. Riccardi, C. Peers, and P. J. Kemp
Hemoxygenase-2 Is an Oxygen Sensor for a Calcium-Sensitive Potassium Channel
Science, December 17, 2004; 306(5704): 2093 - 2097.
[Abstract] [Full Text] [PDF]

Home page
 Cardiovasc ResHome page
S. T. Brown, R. P. Johnson, R. Senaratne, and I. M. Fearon
Amyloid {beta} peptides mediate physiological remodelling of the acute O2 sensitivity of adrenomedullary chromaffin cells following chronic hypoxia
Cardiovasc Res, December 1, 2004; 64(3): 536 - 543.
[Abstract] [Full Text] [PDF]

Home page
 J. Physiol.Home page
M. G Jonz, I. M Fearon, and C. A Nurse
Neuroepithelial oxygen chemoreceptors of the zebrafish gill
J. Physiol., November 1, 2004; 560(3): 737 - 752.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Cell Physiol.Home page
R. P. Johnson, I. M. O'Kelly, and I. M. Fearon
System-specific O2 sensitivity of the tandem pore domain K+ channel TASK-1
Am J Physiol Cell Physiol, February 1, 2004; 286(2): C391 - C397.
[Abstract] [Full Text]

Home page
 J. Appl. Physiol.Home page
J. A. Neubauer and J. Sunderram
Oxygen-sensing neurons in the central nervous system
J Appl Physiol, January 1, 2004; 96(1): 367 - 374.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
M. E. Hartness, S. P. Brazier, C. Peers, A. N. Bateson, M. L. J. Ashford, and P. J. Kemp
Post-transcriptional Control of Human maxiK Potassium Channel Activity and Acute Oxygen Sensitivity by Chronic Hypoxia
J. Biol. Chem., December 19, 2003; 278(51): 51422 - 51432.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Regul. Integr. Comp. Physiol.Home page
W. M. St.-John, I. A. Rybak, and J. F. R. Paton
Potential switch from eupnea to fictive gasping after blockade of glycine transmission and potassium channels
Am J Physiol Regulatory Integrative Comp Physiol, September 1, 2002; 283(3): R721 - R731.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Cell Physiol.Home page
D. J. Keating, G. Y. Rychkov, and M. L. Roberts
Oxygen sensitivity in the sheep adrenal medulla: role of SK channels
Am J Physiol Cell Physiol, November 1, 2001; 281(5): C1434 - C1441.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Cell Physiol.Home page
M. Inoue, N. Fujishiro, and I. Imanaga
Retardation of cation channel deactivation by mitochondrial dysfunction in adrenal medullary cells
Am J Physiol Cell Physiol, January 1, 2000; 278(1): C26 - C32.
[Abstract] [Full Text] [PDF]

Home page
 J. Physiol.Home page
A. Lewis, C. Peers, M. L. J. Ashford, and P. J. Kemp
Hypoxia inhibits human recombinant large conductance, Ca2+-activated K+ (maxi-K) channels by a mechanism which is membrane delimited and Ca2+ sensitive
J. Physiol., May 1, 2002; 540(3): 771 - 780.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1998 The Physiological Society.