Defective Excitation-Contraction Coupling in Experimental Cardiac Hypertrophy and Heart Failure-Reference-Cited by-同舟云学术

Defective Excitation-Contraction Coupling in Experimental Cardiac Hypertrophy and Heart Failure

Published:1997-05-02 Issue:5313 Volume:276 Page:800-806
ISSN:0036-8075
Container-title:Science
language:en
Short-container-title:Science

Author:

Gómez A. M.¹²³⁴⁵,Valdivia H. H.¹²³⁴⁵,Cheng H.¹²³⁴⁵,Lederer Miriam R.¹²³⁴⁵,Santana L. F.¹²³⁴⁵,Cannell M. B.¹²³⁴⁵,McCune S. A.¹²³⁴⁵,Altschuld R. A.¹²³⁴⁵,Lederer W. J.¹²³⁴⁵

Affiliation:

1. A. M. Gómez, L. F. Santana, W. J. Lederer, Department of Physiology and the Medical Biotechnology Center, University of Maryland School of Medicine, 725 West Lombard Street, Baltimore, MD 21201, USA.

2. H. H. Valdivia, Department of Physiology, University of Wisconsin Medical School, Madison, WI 53706, USA.

3. H. Cheng, Medical Biotechnology Center, University of Maryland School of Medicine, 725 West Lombard Street, Baltimore, MD 21201, and Section of Cardiovascular Research, National Institute of Aging, Baltimore, MD 21224, USA.

4. M. R. Lederer, Department of Physiology, University of Maryland School of Medicine, 725 West Lombard Street, Baltimore, MD 21201, USA.

5. M. B. Cannell, Department of Physiology and the Medical Biotechnology Center, University of Maryland School of Medicine, 725 West Lombard Street, Baltimore, MD 21201, USA, and Department of Pharmacology and Clinical Pharmacology, St. George’s Hospital Medical School, London SW17 ORE, UK.

Abstract

Cardiac hypertrophy and heart failure caused by high blood pressure were studied in single myocytes taken from hypertensive rats (Dahl SS/Jr) and SH-HF rats in heart failure. Confocal microscopy and patch-clamp methods were used to examine excitation-contraction (EC) coupling, and the relation between the plasma membrane calcium current ( I Ca ) and evoked calcium release from the sarcoplasmic reticulum (SR), which was visualized as “calcium sparks.” The ability of I Ca to trigger calcium release from the SR in both hypertrophied and failing hearts was reduced. Because I Ca density and SR calcium-release channels were normal, the defect appears to reside in a change in the relation between SR calcium-release channels and sarcolemmal calcium channels. β-Adrenergic stimulation largely overcame the defect in hypertrophic but not failing heart cells. Thus, the same defect in EC coupling that develops during hypertrophy may contribute to heart failure when compensatory mechanisms fail.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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