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


     

J Physiol Vol 491, Issue Pt 1 pp 1-12
Copyright © 1996 by The Physiological Society
This Article
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 Koliwad, S K
Right arrow Articles by Elliott, S J
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Koliwad, S K
Right arrow Articles by Elliott, S J

Oxidant stress activates a non-selective cation channel responsible for membrane depolarization in calf vascular endothelial cells.

 S K Koliwad, D L Kunze and S J Elliott

Department of Molecular Physiology, Baylor College of Medicine, Houston, TX 77030, USA.

1. In vascular endothelial cells, oxidant stress increases cell Na+ content and inhibits the agonist-stimulated influx of external Ca2+. Further, oxidant stress increases uptake of Ca2+ into otherwise quiescent endothelial cells. To determine the mechanism responsible for altered Na+ and Ca2+ homeostasis, the present study examined the effect of oxidant stress on ionic current and channel activity in calf pulmonary artery endothelial cells. 2. Voltage-clamped control cells had a zero-current potential of -60 mV. Incubation of cells with the oxidant tert-butylhydroperoxide (tBuOOH; 0.4 mM, 1 h) caused depolarization to -4 mV and activation of ionic current equally selective for Na+ and K+. 3. Cell-attached membrane patches made on tBuOOH-treated cells contained ion channels that had a bidirectional conductance of 30 pS and that were not present in patches from control cells. Inside-out patches excised from oxidant-treated cells showed the channel to be equally selective for Na+ and K+ and to allow inward Ca2+ current. 4. Oxidant-activated channels were observed to display two gating modalities that were further evident during analysis of single-channel open probability. Neither modality was significantly affected by altering internal [Ca2+] (1 microM-10 nM). 5. Activation of non-selective channels provides a possible mechanism by which oxidants may increase endothelial cell Na+ content. Channel permeability to Ca2+ may account in part for the elevation of cytosolic free [Ca2+] that occurs in oxidant-treated cells. 6. Channel activation is associated with membrane depolarization, a mechanism that may contribute to oxidant inhibition of the agonist-stimulated Ca2+ influx pathway.




This article has been cited by other articles:


Home page
 Am. J. Physiol. Cell Physiol.Home page
F. Simon, D. Varela, A. L. Eguiguren, L. F. Diaz, F. Sala, and A. Stutzin
Hydroxyl radical activation of a Ca2+-sensitive nonselective cation channel involved in epithelial cell necrosis
Am J Physiol Cell Physiol, October 1, 2004; 287(4): C963 - C970.
[Abstract] [Full Text] [PDF]

Home page
 Cardiovasc ResHome page
M. Balzer, B. Lintschinger, and K. Groschner
Evidence for a role of Trp proteins in the oxidative stress-induced membrane conductances of porcine aortic endothelial cells
Cardiovasc Res, May 1, 1999; 42(2): 543 - 549.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1996 The Physiological Society.