Lysophospholipid-mediated alterations in the calcium transport systems of skeletal and cardiac muscle sarcoplasmic reticulum

1988 ◽  
Vol 79 (1) ◽  
pp. 81-89 ◽  
Author(s):  
Indu S. Ambudkar ◽  
El-Sayed Abdallah ◽  
Adil E. Shamoo
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Cardiac Muscle ◽  
Calcium Transport ◽  
Transport Systems

Regulation of calcium transport in cardiac cells

1984 ◽  
Vol 62 (1) ◽  
pp. 9-22 ◽  
Author(s):  
Adil E. Shamoo ◽  
Indu S. Ambudkar
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Calcium Channel ◽  
Calcium Homeostasis ◽  
Calcium Transport ◽  
Cardiac Cells ◽  
Transport Systems ◽  
Sodium Calcium Exchanger ◽  
Inotropic Effects ◽  
Cellular Calcium ◽  
Sodium Calcium

Calcium transporting systems and the regulatory events accompanying them are pivotal in the function of the cardiac cell. The concerted involvement of the various membranes achieve cellular calcium homeostasis that can also respond to the physiological exigencies of the cell. Three membrane systems are primarily involved; the sarcolemma, sarcoplasmic reticulum, and the mitochondria. The various Ca2+ transport systems that have been described in these membranes are as follows: the calcium channel, Ca2+-ATPase, Ca2+–Mg2+ ATPase, and sodium–calcium exchanger in the sarcolemma; the Ca2+–Mg2+ ATPase and a possible calcium channel in the sarcoplasmic reticulum; and the sodium–calcium exchanger and electrophoretic calcium uniporter in the mitochondrial inner membrane. These systems mediate calcium fluxes to maintain physiological cytosolic calcium concentrations. β-Adrenergic hormones regulate calcium transport systems in sarcolemma and sarcoplasmic reticulum, while α-adrenergic hormones modulate those in the mitochondria and probably in the sarcolemma. The response to these hormones is initiated at the sarcolemma, which contains the specific receptors. Intracellularly the effects are propagated by secondary messengers, e.g., cAMP, calcium, and lipid changes. Specific proteins are also involved in these events. Phospholamban, a 22 000 dalton protein, is involved in mediating the cAMP-dependent inotropic effects, by activating the Ca2+–Mg2+ ATPase of the sarcoplasmic reticulum. Alterations in any one of the systems involved in the regulation of calcium transport or in the calcium transport systems per se, would then result in drastic alterations in the cellular calcium homeostasis. Such effects could be of significance in cellular dysfunction during cardiac disease.

scholarly journals The Effect of Quinidine on Calcium Accumulation by Isolated Sarcoplasmic Reticulum of Skeletal and Cardiac Muscle

1968 ◽  
Vol 52 (6) ◽  
pp. 955-968 ◽  
Author(s):  
Franklin Fuchs ◽  
Edward W. Gertz ◽  
F. Norman Briggs
Keyword(s):  
Skeletal Muscle ◽  
Sarcoplasmic Reticulum ◽  
Cardiac Muscle ◽  
Calcium Transport ◽  
Coupling Mechanism ◽  
Muscle Preparation ◽  
Cardiac Sarcoplasmic Reticulum ◽  
Tension Development ◽  
Calcium Accumulation ◽  
Pharmacologically Active

Quinidine potentiates twitch tension and (at higher concentrations) causes contracture of skeletal muscle whereas the same drug reduces tension development of cardiac muscle. To gain insight into the possible differences in the excitation-contraction coupling mechanism of the two types of muscle the effect of quinidine on calcium accumulation by isolated sarcoplasmic reticulum from skeletal and cardiac muscle was investigated. In a medium containing ATP, Mg++, oxalate, and 45Ca, pharmacologically active concentrations of the drug inhibited calcium accumulation by both skeletal and cardiac sarcoplasmic reticulum. The inhibition of the rates of calcium, uptake by the skeletal muscle preparation ranged from 11% with 10-4M quinidine to 90% with 10-3 M quinidine. With the cardiac muscle preparation the inhibition ranged from 16% with 3 x 10-6 M quinidine to 100% with 10-3 M quinidine. With both preparations the inhibition of calcium transport was accompanied by an inhibition of the Ca++-activated ATPase activity of the sarcoplasmic reticulum. The effect of quinidine on the skeletal sarcoplasmic reticulum supports the hypothesis that this compound produces twitch potentiation and contracture by interfering with intracellular calcium, sequestration. Its effect on cardiac sarcoplasmic reticulum. has been interpreted in terms of the hypothesis that cardiac contractility is a function of the amount of calcium released from the sarcoplasmic reticulum which is in turn dependent upon the absolute calcium content of the reticulum. Hence, following inhibition of calcium transport there would be less calcium available for coupling.

Anchorfibers and the Topography of Junctional SR

1977 ◽  
Vol 35 ◽  
pp. 582-583
Author(s):  
James Junker ◽  
Joachim R. Sommer
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Cardiac Muscle ◽  
Single Filament ◽  
Relaxation Cycle ◽  
10 Nm Filaments ◽  
Junctional Sarcoplasmic Reticulum

Junctional sarcoplasmic reticulum (JSR) in all its forms (extended JSR, JSR of couplings, corbular SR) in both skeletal and cardiac muscle is always located at the Z - I regions of the sarcomeres. The Z tubule is a tubule of the free SR (non-specialized SR) which is consistently located at the Z lines in cardiac muscle (1). Short connections between JSR and Z lines have been described (2), and bundles of filaments at Z lines have been seen in skeletal (3) and cardiac (4) muscle. In opossum cardiac muscle, we have seen bundles of 10 nm filaments stretching across interfibrillary spaces and adjacent myofibrils with extensions to the plasma- lemma in longitudinal (Fig. 1) and transverse (Fig. 2) sections. Only an occasional single filament is seen elsewhere along a sarcomere. We propose that these filaments represent anchor fibers that maintain the observed invariant topography of the free SR and JSR throughout the contraction-relaxation cycle.

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