scholarly journals Response: Does Voltage Affect Excitation-Contraction Coupling in the Heart?

Science ◽  
1989 ◽  
Vol 246 (4937) ◽  
pp. 1640-1640
Author(s):  
M. MORAD ◽  
L. CLEEMANN ◽  
G. CALLAWAERT
Keyword(s):  
Excitation Contraction Coupling ◽  
Contraction Coupling

scholarly journals Remodeling of t-system and proteins underlying excitation-contraction coupling in aging versus failing human heart

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Yankun Lyu ◽  
Vipin K. Verma ◽  
Younjee Lee ◽  
Iosif Taleb ◽  
Rachit Badolia ◽  
...  
Keyword(s):  
Heart Function ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Left Ventricular Myocardium ◽  
Excitation Contraction Coupling ◽  
Transverse Tubular System ◽  
Contraction Coupling ◽  
Senescent Phenotype ◽  
Cellular Microstructure ◽  
T System

AbstractIt is well established that the aging heart progressively remodels towards a senescent phenotype, but alterations of cellular microstructure and their differences to chronic heart failure (HF) associated remodeling remain ill-defined. Here, we show that the transverse tubular system (t-system) and proteins underlying excitation-contraction coupling in cardiomyocytes are characteristically remodeled with age. We shed light on mechanisms of this remodeling and identified similarities and differences to chronic HF. Using left ventricular myocardium from donors and HF patients with ages between 19 and 75 years, we established a library of 3D reconstructions of the t-system as well as ryanodine receptor (RyR) and junctophilin 2 (JPH2) clusters. Aging was characterized by t-system alterations and sarcolemmal dissociation of RyR clusters. This remodeling was less pronounced than in HF and accompanied by major alterations of JPH2 arrangement. Our study indicates that targeting sarcolemmal association of JPH2 might ameliorate age-associated deficiencies of heart function.

scholarly journals 112 THE AGE DEPENDENCY OF MYOCARDIAL EXCITATION CONTRACTION COUPLING

1985 ◽  
Vol 19 (4) ◽  
pp. 129A-129A
Author(s):  
Thomas S Klitzner ◽  
William F Friedman
Keyword(s):  
Age Dependency ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling

scholarly journals Age and gender differences in excitation-contraction coupling of the rat ventricle

1998 ◽  
Vol 511 (2) ◽  
pp. 533-548 ◽  
Author(s):  
Normand Leblanc ◽  
Denis Chartier ◽  
Hugues Gosselin ◽  
Jean-Lucien Rouleau
Keyword(s):  
Gender Differences ◽  
Age And Gender ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling ◽  
Age And Gender Differences ◽  
And Gender ◽  
Rat Ventricle

scholarly journals Myocardial Excitation-contraction Coupling in the Fetus of Alloxan-diabetic Rabbit

1984 ◽  
Vol 18 (12) ◽  
pp. 1344-1349 ◽  
Author(s):  
Toshio Nakanishi ◽  
Suguru Matsuoka ◽  
Shigeru Uemura ◽  
Tatsuo Shimizu ◽  
Kenya Nishioka ◽  
...  
Keyword(s):  
Excitation Contraction Coupling ◽  
Contraction Coupling ◽  
Diabetic Rabbit

scholarly journals Effects of mitochondrial uncoupling on Ca2+ signaling during excitation-contraction coupling in atrial myocytes

2013 ◽  
Vol 304 (7) ◽  
pp. H983-H993 ◽  
Author(s):  
Aleksey V. Zima ◽  
Malikarjuna R. Pabbidi ◽  
Stephen L. Lipsius ◽  
Lothar A. Blatter
Keyword(s):  
Ion Homeostasis ◽  
Inhibitory Effect ◽  
Partial Recovery ◽  
Atrial Myocytes ◽  
Mitochondrial Uncoupling ◽  
Release Channel ◽  
Excitation Contraction Coupling ◽  
Atp Production ◽  
Contraction Coupling ◽  
Reverse Mode

Mitochondria play an important role in intracellular Ca2+ concentration ([Ca2+]i) regulation in the heart. We studied sarcoplasmic reticulum (SR) Ca2+ release in cat atrial myocytes during depolarization of mitochondrial membrane potential (ΔΨm) induced by the protonophore FCCP. FCCP caused an initial decrease of action potential-induced Ca2+ transient amplitude and frequency of spontaneous Ca2+ waves followed by partial recovery despite partially depleted SR Ca2+ stores. In the presence of oligomycin, FCCP only exerted a stimulatory effect on Ca2+ transients and Ca2+ wave frequency, suggesting that the inhibitory effect of FCCP was mediated by ATP consumption through reverse-mode operation of mitochondrial F1F0-ATPase. ΔΨm depolarization was accompanied by cytosolic acidification, increases of diastolic [Ca2+]i, intracellular Na+ concentration ([Na+]i), and intracellular Mg2+ concentration ([Mg2+]i), and a decrease of intracellular ATP concentration ([ATP]i); however, glycolytic ATP production partially compensated for the exhaustion of mitochondrial ATP supplies. In conclusion, the initial inhibition of Ca2+ transients and waves resulted from suppression of ryanodine receptor SR Ca2+ release channel activity by a decrease in [ATP], an increase of [Mg2+]i, and cytoplasmic acidification. The later stimulation resulted from reduced mitochondrial Ca2+ buffering and cytosolic Na+ and Ca2+ accumulation, leading to enhanced Ca2+-induced Ca2+ release and spontaneous Ca2+ release in the form of Ca2+ waves. ΔΨm depolarization and the ensuing consequences of mitochondrial uncoupling observed here (intracellular acidification, decrease of [ATP]i, increase of [Na+]i and [Mg2+]i, and Ca2+ overload) are hallmarks of ischemia. These findings may therefore provide insight into the consequences of mitochondrial uncoupling for ion homeostasis, SR Ca2+ release, and excitation-contraction coupling in ischemia at the cellular and subcellular level.

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