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Metabolic stress in isolated mouse ventricular myocytes leads to remodeling of t tubules

Metabolic stress in isolated mouse ventricular myocytes leads to remodeling of t tubules Abstract Cardiac ventricular myocytes possess an extensive t-tubular system that facilitates the propagation of membrane potential across the cell body. It is well established that ionic currents at the restricted t-tubular space may lead to significant changes in ion concentrations, which, in turn, may affect t-tubular membrane potential. In this study, we used the whole cell patch-clamp technique to study accumulation and depletion of t-tubular potassium by measuring inward rectifier potassium tail currents ( I K1,tail ), and inward rectifier potassium current ( I K1 ) “inactivation”. At room temperatures and in the absence of Mg 2+ ions in pipette solution, the amplitude of I K1,tail measured ∼10 min after the establishment of whole cell configuration was reduced by ∼18%, but declined nearly twofold in the presence of 1 mM cyanide. At ∼35°C I K1,tail was essentially preserved in intact cells, but its amplitude declined by ∼85% within 5 min of cell dialysis, even in the absence of cyanide. Intracellular Mg 2+ ions played protective role at all temperatures. Decline of I K1,tail was accompanied by characteristic changes in its kinetics, as well as by changes in the kinetics of I K1 inactivation, a marker of depletion of t-tubular K + . The data point to remodeling of t tubules as the primary reason for the observed effects. Consistent with this, detubulation of myocytes using formamide-induced osmotic stress significantly reduced I K1,tail , as well as the inactivation of inward I K1 . Overall, the data provide strong evidence that changes in t tubule volume/structure may occur on a short time scale in response to various types of stress. inward rectifier potassium channels cardiac myocytes Copyright © 2011 the American Physiological Society « Previous | Next Article » Table of Contents This Article Published online before print September 2011 , doi: 10.​1152/​ajpheart.​00304.​2011 AJP - Heart November 2011 vol. 301 no. 5 H1984-H1995 » Abstract Free Full Text Free to you Full Text (PDF) Free to you All Versions of this Article: ajpheart.00304.2011v1 301/5/H1984 most recent Classifications Cardiac Excitation and Contraction Services Email this article to a friend Alert me when this article is cited Alert me if a correction is posted Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Download to citation manager Citing Articles Load citing article information Citing articles via Web of Science Google Scholar Articles by Cheng, L. Articles by Lopatin, A. N. PubMed PubMed citation Articles by Cheng, L. Articles by Lopatin, A. N. Related Content Cardiac Excitation and Contraction Load related web page information Current Issue November 2011, 301 (5) Alert me to new issues of AJP - Heart About the Journal Information for Authors Submit a Manuscript Ethical Policies AuthorChoice PubMed Central Policy Reprints and Permissions Advertising Press Copyright © 2011 the American Physiological Society Print ISSN: 0363-6135 Online ISSN: 1522-1539 var gaJsHost = (("https:" == document.location.protocol) ? "https://ssl." : "http://www."); document.write(unescape("%3Cscript src='" + gaJsHost + "google-analytics.com/ga.js' type='text/javascript'%3E%3C/script%3E")); var pageTracker = _gat._getTracker("UA-2924550-1"); pageTracker._trackPageview(); http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png AJP - Heart and Circulatory Physiology The American Physiological Society

Metabolic stress in isolated mouse ventricular myocytes leads to remodeling of t tubules

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References (33)

Publisher
The American Physiological Society
Copyright
Copyright © 2011 the American Physiological Society
ISSN
0363-6135
eISSN
1522-1539
DOI
10.1152/ajpheart.00304.2011
pmid
21890686
Publisher site
See Article on Publisher Site

Abstract

Abstract Cardiac ventricular myocytes possess an extensive t-tubular system that facilitates the propagation of membrane potential across the cell body. It is well established that ionic currents at the restricted t-tubular space may lead to significant changes in ion concentrations, which, in turn, may affect t-tubular membrane potential. In this study, we used the whole cell patch-clamp technique to study accumulation and depletion of t-tubular potassium by measuring inward rectifier potassium tail currents ( I K1,tail ), and inward rectifier potassium current ( I K1 ) “inactivation”. At room temperatures and in the absence of Mg 2+ ions in pipette solution, the amplitude of I K1,tail measured ∼10 min after the establishment of whole cell configuration was reduced by ∼18%, but declined nearly twofold in the presence of 1 mM cyanide. At ∼35°C I K1,tail was essentially preserved in intact cells, but its amplitude declined by ∼85% within 5 min of cell dialysis, even in the absence of cyanide. Intracellular Mg 2+ ions played protective role at all temperatures. Decline of I K1,tail was accompanied by characteristic changes in its kinetics, as well as by changes in the kinetics of I K1 inactivation, a marker of depletion of t-tubular K + . The data point to remodeling of t tubules as the primary reason for the observed effects. Consistent with this, detubulation of myocytes using formamide-induced osmotic stress significantly reduced I K1,tail , as well as the inactivation of inward I K1 . Overall, the data provide strong evidence that changes in t tubule volume/structure may occur on a short time scale in response to various types of stress. inward rectifier potassium channels cardiac myocytes Copyright © 2011 the American Physiological Society « Previous | Next Article » Table of Contents This Article Published online before print September 2011 , doi: 10.​1152/​ajpheart.​00304.​2011 AJP - Heart November 2011 vol. 301 no. 5 H1984-H1995 » Abstract Free Full Text Free to you Full Text (PDF) Free to you All Versions of this Article: ajpheart.00304.2011v1 301/5/H1984 most recent Classifications Cardiac Excitation and Contraction Services Email this article to a friend Alert me when this article is cited Alert me if a correction is posted Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Download to citation manager Citing Articles Load citing article information Citing articles via Web of Science Google Scholar Articles by Cheng, L. Articles by Lopatin, A. N. PubMed PubMed citation Articles by Cheng, L. Articles by Lopatin, A. N. Related Content Cardiac Excitation and Contraction Load related web page information Current Issue November 2011, 301 (5) Alert me to new issues of AJP - Heart About the Journal Information for Authors Submit a Manuscript Ethical Policies AuthorChoice PubMed Central Policy Reprints and Permissions Advertising Press Copyright © 2011 the American Physiological Society Print ISSN: 0363-6135 Online ISSN: 1522-1539 var gaJsHost = (("https:" == document.location.protocol) ? "https://ssl." : "http://www."); document.write(unescape("%3Cscript src='" + gaJsHost + "google-analytics.com/ga.js' type='text/javascript'%3E%3C/script%3E")); var pageTracker = _gat._getTracker("UA-2924550-1"); pageTracker._trackPageview();

Journal

AJP - Heart and Circulatory PhysiologyThe American Physiological Society

Published: Nov 1, 2011

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