Regulation of cardiac L-type Ca2+ current in Na+-Ca2+ exchanger knockout mice: functional coupling of the Ca2+ channel and the Na+-Ca2+ exchanger.

Regulation of cardiac L-type Ca2+ current in Na+-Ca2+ exchanger knockout mice: functional coupling of the Ca2+ channel and the Na+-Ca2+ exchanger. Research Abstract Details 

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Regulation of cardiac L-type Ca2+ current in Na+-Ca2+ exchanger knockout mice: functional coupling of the Ca2+ channel and the Na+-Ca2+ exchanger. Abstract Text:

Christian Pott,Mey Yip,Joshua I Goldhaber,Kenneth D Philipson,

L-type Ca2+ current (I(Ca)) is reduced in myocytes from cardiac-specific Na+-Ca2+ exchanger (NCX) knockout (KO) mice. This is an important adaptation to prevent Ca2+ overload in the absence of NCX. However, Ca2+ channel expression is unchanged, suggesting that regulatory processes reduce I(Ca). We tested the hypothesis that an elevation in local Ca2+ reduces I(Ca) in KO myocytes. In patch-clamped myocytes from NCX KO mice, peak I(Ca) was reduced by 50%, and inactivation kinetics were accelerated as compared to wild-type (WT) myocytes. To assess the effects of cytosolic Ca2+ concentration on I(Ca), we used Ba2+ instead of Ca2+ as the charge carrier and simultaneously depleted sarcoplasmic reticular Ca2+ with thapsigargin and ryanodine. Under these conditions, we observed no significant difference in Ba2+ current between WT and KO myocytes. Also, dialysis with the fast Ca2+ chelator BAPTA eliminated differences in both I(Ca) amplitude and decay kinetics between KO and WT myocytes. We conclude that, in NCX KO myocytes, Ca2+-dependent inactivation of I(Ca) reduces I(Ca) amplitude and accelerates current decay kinetics. We hypothesize that the elevated subsarcolemmal Ca2+ that results from the absence of NCX activity inactivates some L-type Ca2+ channels. Modulation of subsarcolemmal Ca2+ by the Na+-Ca2+ exchanger may be an important regulator of excitation-contraction coupling.

Regulation of cardiac L-type Ca2+ current in Na+-Ca2+ exchanger knockout mice: functional coupling of the Ca2+ channel and the Na+-Ca2+ exchanger. Publishing Authors By Initials

C Pott,M Yip,JI Goldhaber,KD Philipson,

For similar proteins: carrier proteins: membrane transport proteins: ion pumps: antiporters: sodium-calcium exchanger research abstracts see: proteins: carrier proteins: membrane transport proteins: ion pumps: antiporters: sodium-calcium exchanger research

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Regulation of cardiac L-type Ca2+ current in Na+-Ca2+ exchanger knockout mice: functional coupling of the Ca2+ channel and the Na+-Ca2+ exchanger. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: Biophysical journal

VOLUME: 92

Page Numbers: 1431-7

Journal Abbreviation: Biophys. J.

ISSN: 0006-3495

DAY: 17

MONTH: 11

YEAR: 2006

Regulation of cardiac L-type Ca2+ current in Na+-Ca2+ exchanger knockout mice: functional coupling of the Ca2+ channel and the Na+-Ca2+ exchanger. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 370626

Regulation of cardiac L-type Ca2+ current in Na+-Ca2+ exchanger knockout mice: functional coupling of the Ca2+ channel and the Na+-Ca2+ exchanger. Keywords Mesh Terms:

KEYWORDS: Sodium-Calcium Exchanger

MESH TERMS: physiology

Chemical & Substance for Abstract: Regulation of cardiac L-type Ca2+ current in Na+-Ca2+ exchanger knockout mice: functional coupling of the Ca2+ channel and the Na+-Ca2+ exchanger. Information

Substance Name: Calcium

Registry Number: 7440-70-2

Grant and Affiliation Information for Regulation of cardiac L-type Ca2+ current in Na+-Ca2+ exchanger knockout mice: functional coupling of the Ca2+ channel and the Na+-Ca2+ exchanger.

AFFILIATION: Department of Physiology, David Geffen School of Medicine at the University of California, Los Angeles, California 90095, USA.

Country: United States

AGENCY: United States NHLBI

GRANT: HL70828

ACRONYM: HL

MEDLINETA: Biophys J

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