Enhanced sarcolemmal Ca2+ efflux reduces sarcoplasmic reticulum Ca2+ content and systolic Ca2+ in cardiac hypertrophy

M. E. Díaz; H. K. Graham; A. W. Trafford

doi:10.1016/j.cardiores.2004.01.038

Enhanced sarcolemmal Ca2+ efflux reduces sarcoplasmic reticulum Ca2+ content and systolic Ca2+ in cardiac hypertrophy

M. E. Díaz, H. K. Graham, A. W. Trafford

Research output: Contribution to journal › Article › peer-review

Abstract

Objective: Recent work has identified reductions in the systolic Ca 2+ transient in cardiac disease states. The aim of the present study was to identify the mechanisms responsible for perturbations of intracellular calcium homeostasis in isolated cardiac myocytes and determine if such changes can quantitatively explain the reduced systolic Ca2+ transient. Methods: Left ventricular hypertrophy (LVH) was induced by aortic coarctation in adult ferrets. Changes in intracellular Ca2+ regulation, sarcolemmal Ca2+ fluxes and SR function were measured in single left ventricular cardiac myocytes. Results: Cardiac hypertrophy was associated with a 29% increase in action potential duration (APD90); a 48% reduction in the amplitude of and 19% slowing in the rate of decay of the systolic Ca 2+ transient; a 20% decrease in SR Ca2+ content and a 36% increase in inward Na+-Ca2+ exchange current for a given change in [Ca2+]i (all P

Original language	English
Pages (from-to)	538-547
Number of pages	9
Journal	Cardiovascular research
Volume	62
Issue number	3
DOIs	https://doi.org/10.1016/j.cardiores.2004.01.038
Publication status	Published - 1 Jun 2004

Keywords

e-C coupling
Hypertrophy
Myocytes
Na/Ca-exchanger
SR (function)

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10.1016/j.cardiores.2004.01.038

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title = "Enhanced sarcolemmal Ca2+ efflux reduces sarcoplasmic reticulum Ca2+ content and systolic Ca2+ in cardiac hypertrophy",

abstract = "Objective: Recent work has identified reductions in the systolic Ca 2+ transient in cardiac disease states. The aim of the present study was to identify the mechanisms responsible for perturbations of intracellular calcium homeostasis in isolated cardiac myocytes and determine if such changes can quantitatively explain the reduced systolic Ca2+ transient. Methods: Left ventricular hypertrophy (LVH) was induced by aortic coarctation in adult ferrets. Changes in intracellular Ca2+ regulation, sarcolemmal Ca2+ fluxes and SR function were measured in single left ventricular cardiac myocytes. Results: Cardiac hypertrophy was associated with a 29% increase in action potential duration (APD90); a 48% reduction in the amplitude of and 19% slowing in the rate of decay of the systolic Ca 2+ transient; a 20% decrease in SR Ca2+ content and a 36% increase in inward Na+-Ca2+ exchange current for a given change in [Ca2+]i (all P",

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T1 - Enhanced sarcolemmal Ca2+ efflux reduces sarcoplasmic reticulum Ca2+ content and systolic Ca2+ in cardiac hypertrophy

AU - Díaz, M. E.

AU - Graham, H. K.

AU - Trafford, A. W.

PY - 2004/6/1

Y1 - 2004/6/1

N2 - Objective: Recent work has identified reductions in the systolic Ca 2+ transient in cardiac disease states. The aim of the present study was to identify the mechanisms responsible for perturbations of intracellular calcium homeostasis in isolated cardiac myocytes and determine if such changes can quantitatively explain the reduced systolic Ca2+ transient. Methods: Left ventricular hypertrophy (LVH) was induced by aortic coarctation in adult ferrets. Changes in intracellular Ca2+ regulation, sarcolemmal Ca2+ fluxes and SR function were measured in single left ventricular cardiac myocytes. Results: Cardiac hypertrophy was associated with a 29% increase in action potential duration (APD90); a 48% reduction in the amplitude of and 19% slowing in the rate of decay of the systolic Ca 2+ transient; a 20% decrease in SR Ca2+ content and a 36% increase in inward Na+-Ca2+ exchange current for a given change in [Ca2+]i (all P

AB - Objective: Recent work has identified reductions in the systolic Ca 2+ transient in cardiac disease states. The aim of the present study was to identify the mechanisms responsible for perturbations of intracellular calcium homeostasis in isolated cardiac myocytes and determine if such changes can quantitatively explain the reduced systolic Ca2+ transient. Methods: Left ventricular hypertrophy (LVH) was induced by aortic coarctation in adult ferrets. Changes in intracellular Ca2+ regulation, sarcolemmal Ca2+ fluxes and SR function were measured in single left ventricular cardiac myocytes. Results: Cardiac hypertrophy was associated with a 29% increase in action potential duration (APD90); a 48% reduction in the amplitude of and 19% slowing in the rate of decay of the systolic Ca 2+ transient; a 20% decrease in SR Ca2+ content and a 36% increase in inward Na+-Ca2+ exchange current for a given change in [Ca2+]i (all P

KW - e-C coupling

KW - Hypertrophy

KW - Myocytes

KW - Na/Ca-exchanger

KW - SR (function)

U2 - 10.1016/j.cardiores.2004.01.038

DO - 10.1016/j.cardiores.2004.01.038

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SN - 0008-6363

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JO - Cardiovascular research

JF - Cardiovascular research

IS - 3

ER -

Enhanced sarcolemmal Ca2+ efflux reduces sarcoplasmic reticulum Ca2+ content and systolic Ca2+ in cardiac hypertrophy

Abstract

Keywords

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