scholarly journals The binding of tritium-labeled cardiac glycosides by sarcoplasmic reticulum and by cell membrane isolated from cat heart

1971 ◽  
Vol 67 (3) ◽  
pp. 252-264
Author(s):  
Shunsaku KAWAGISHI
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Cell Membrane ◽  
Cardiac Glycosides ◽  
Cat Heart

Ouabain potentiation and Ca release from sarcoplasmic reticulum in cardiac and skeletal muscle cells

1982 ◽  
Vol 60 (4) ◽  
pp. 542-555 ◽  
Author(s):  
S. Fujino ◽  
M. Fujino
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Guinea Pig ◽  
Skeletal Muscles ◽  
Cardiac Glycosides ◽  
Positive Inotropic Effect ◽  
Frog Heart ◽  
Heart Ventricle ◽  
Guinea Pig Heart ◽  
Intracellular Mechanism ◽  
Cat Heart

In this article, we describe a possible mechanism of ouabain potentiation in heart based on the following findings in cardiac and skeletal muscles of various species. (1) In heart ventricle muscles of frog and guinea pig, the ouabain potentiation is produced without an effect on Ca influx. In both frog and cat heart ventricle muscles, ouabain potentiates the rapid cooling contracture with or without caffeine in a Ca-deprived medium. It follows, therefore, that the ouabain potentiation is produced by an "intracellular" mechanism. (2) In crab single muscle fibers, contractile responses such as twitch, potassium-induced contracture, caffeine-induced contracture, and water-induced contracture are remarkably potentiated if ouabain is present within the fibers by microinjection, whereas the situation is reversed if the drug is given extracellularly. (3) The ouabain potentiated the Ca release from fragmented sarcoplasmic reticulum (FSR) isolated from cat, guinea pig, and frog heart and from skeletal muscles as a result of the procedures used, such as changing the ionic environment. (4) In frog, cat, and guinea pig heart ventricle muscles, a reduction of contractility as a result of pretreatment with urea–Ringer's was completely cancelled by ouabain almost without influencing the membrane depolarization. Based on these findings and others, the deduction was made that the positive inotropic effect of cardiac glycosides on the heart is brought about by potentiation of contraction – Ca release from the intracellular store sites, namely the sarcoplasmic reticulum.

Stimulatory effect of vanadate on (Na+ + K+)-ATPase activity and on 3H-ouabain-binding in a cat heart cell membrane preparation

Nature ◽  
1979 ◽  
Vol 278 (5703) ◽  
pp. 459-461 ◽  
Author(s):  
ERLAND ERDMANN ◽  
WOLFGANG KRAWIETZ ◽  
GUNTHER PHILIPP ◽  
INGELORE HACKBARTH ◽  
WILHELM SCHMITZ ◽  
...  
Keyword(s):  
Cell Membrane ◽  
Atpase Activity ◽  
Membrane Preparation ◽  
Heart Cell ◽  
Ouabain Binding ◽  
Heart Cell Membrane ◽  
Cell Membrane Preparation ◽  
Cat Heart

Postrest inotropy in rabbit ventricle: Na+-Ca2+ exchange determines sarcoplasmic reticulum Ca2+ content

1986 ◽  
Vol 250 (4) ◽  
pp. H654-H661 ◽  
Author(s):  
J. L. Sutko ◽  
D. M. Bers ◽  
J. P. Reeves
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Cardiac Muscle ◽  
Cardiac Glycosides ◽  
General Increase ◽  
Rhythmic Stimulation ◽  
Na Pump ◽  
Inotropic State ◽  
Rest Periods ◽  
Efflux Mechanism ◽  
Efflux Pathway

To determine whether Na+-Ca2+ exchange is a physiologically significant Ca2+ efflux mechanism in rabbit ventricle, we investigated the effects exerted on postrest contractions by interventions that alter the transmembrane distribution of Na+ or Ca2+ so as to retard Ca2+ efflux via this system. Contractions elicited after rest periods of 0.25-10 min in duration were studied. The following interventions increased postrest contractions much more than those elicited by rhythmic stimulation: 1) Na+ pump inhibition by cardiac glycosides or by a reduction in extracellular K+, 2) reduction of extracellular Na+ (maintaining a constant [Ca2+]-to-[Na+]2 ratio), and 3) elevation of extracellular Ca2+. In contrast, isoproterenol, norepinephrine, and histamine produced comparable increases in both rhythmically stimulated and postrest contractions, suggesting that the postrest contractile potentiation was not just the result of a general increase in inotropic state. Ryanodine, which appears to antagonize sarcoplasmic reticulum (SR) Ca2+ release in cardiac muscle, markedly reduced the amplitude of the postrest contractions, but only modestly decreased rhythmically stimulated responses. Results suggest 1) that Ca2+ released from SR is involved in postrest response, 2) that Na+-Ca2+ exchange serves as a Ca2+ efflux pathway in normally polarized resting rabbit ventricle, and 3) that this activity in part determines the amount of Ca2+ available for release from SR.

scholarly journals There Goes the Neighborhood: Pathological Alterations in T-Tubule Morphology and Consequences for Cardiomyocyte Handling

2010 ◽  
Vol 2010 ◽  
pp. 1-17 ◽  
Author(s):  
William E. Louch ◽  
Ole M. Sejersted ◽  
Fredrik Swift
Keyword(s):  
Heart Failure ◽  
Atrial Fibrillation ◽  
Sarcoplasmic Reticulum ◽  
Cell Membrane ◽  
Diabetic Cardiomyopathy ◽  
Tight Coupling ◽  
Cell Interior ◽  
Intracellular Store ◽  
T Tubules ◽  
Novel Therapeutic

T-tubules are invaginations of the cardiomyocyte membrane into the cell interior which form a tortuous network. T-tubules provide proximity between the electrically excitable cell membrane and the sarcoplasmic reticulum, the main intracellular store. Tight coupling between the rapidly spreading action potential and release units in the SR membrane ensures synchronous release throughout the cardiomyocyte. This is a requirement for rapid and powerful contraction. In recent years, it has become clear that T-tubule structure and composition are altered in several pathological states which may importantly contribute to contractile defects in these conditions. In this review, we describe the “neighborhood” of proteins in the dyadic cleft which locally controls cardiomyocyte homeostasis and how alterations in T-tubule structure and composition may alter this neighborhood during heart failure, atrial fibrillation, and diabetic cardiomyopathy. Based on this evidence, we propose that T-tubules have the potential to serve as novel therapeutic targets.

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