scholarly journals What is the purpose of the large sarcolemmal calcium flux on each heartbeat?

2009 ◽  
Vol 297 (2) ◽  
pp. H493-H494 ◽  
Author(s):  
D. A. Eisner ◽  
A. W. Trafford
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Cardiac Muscle ◽  
Calcium Release ◽  
Calcium Influx ◽  
Calcium Content ◽  
Significant Fraction ◽  
Alternative Strategy ◽  
Calcium Flux ◽  
Rapid Changes ◽  
Inotropic Responses

In cardiac muscle, although most of the calcium that activates contraction comes from the sarcoplasmic reticulum (SR), a significant fraction (up to 30%, depending on the species) enters from outside the cell and is then pumped out at the end of systole. Although some of this calcium influx is required to trigger calcium release from the SR, the bulk serves to reload the cell (and thence the SR) with calcium to replace the calcium that is pumped out of the cell. An alternative strategy would be for the heart to have a much smaller calcium influx balancing a smaller efflux. We demonstrate that this would result in a slowing of inotropic responses due to changes of SR calcium content. We conclude that the large sarcolemmal calcium fluxes facilitate rapid changes of contractility.

Direct Measurement of Sarcoplasmic Reticulum Calcium Content Following Isoproterenol or Caffeine Treatment

1997 ◽  
Vol 3 (S2) ◽  
pp. 919-920
Author(s):  
Wendy E. Sweet ◽  
Christine S. Moravec
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Cardiac Muscle ◽  
Calcium Release ◽  
Calcium Influx ◽  
Calcium Content ◽  
Storage Site ◽  
Calcium Store ◽  
Indirect Methods ◽  
Β Receptor ◽  
Sarcoplasmic Reticulum Calcium

The major storage site for calcium in cardiac muscle is the sarcoplasmic reticulum (SR). It has been shown using indirect methods that the amount of calcium stored in the SR can be altered by various agonists and anesthetics. The only technique to date which directly quantifies the amount of calcium in the SR is Electron Probe Microanalysis (EPMA). Using EPMA, an accurate measurement of the size of the SR calcium store can be made following treatments with known agonists.Isoproterenol (ISO) causes an increased inotropic response in cardiac muscle via the (3-adrenergic pathway. When ISO binds to the (β-receptor on the plasma membrane, it causes the activation of Protein Kinase A (PKA) through a cascade of events. PKA phosphorylates the sarcolemmal calcium channels causing an increase in the rate of calcium influx. PKA also phosphorylates Tnl, which sensitizes the myofilaments to calcium, thereby increasing the rate of calcium release from the myofilaments.

scholarly journals Phosphorylation Modulates the Function of the Calcium Release Channel of Sarcoplasmic Reticulum from Cardiac Muscle

1995 ◽  
Vol 270 (5) ◽  
pp. 2074-2081 ◽  
Author(s):  
Jürgen Hain ◽  
Hitoshi Onoue ◽  
Martin Mayrleitner ◽  
Sidney Fleischer ◽  
Hansgeorg Schindler
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Cardiac Muscle ◽  
Calcium Release ◽  
Calcium Release Channel ◽  
Release Channel

The Anatomy of the Sarcoplasmic Reticulum in Vertebrate Skeletal Muscle: Its Implications for Excitation Contraction Coupling

1982 ◽  
Vol 37 (7-8) ◽  
pp. 665-678 ◽  
Author(s):  
Joachim R. Sommer
Keyword(s):  
Skeletal Muscle ◽  
Sarcoplasmic Reticulum ◽  
Action Potential ◽  
Cardiac Muscle ◽  
Calcium Release ◽  
Striated Muscle ◽  
Band Region ◽  
Terminal Cisterna ◽  
Transmitter Substance ◽  
Main Components

Abstract The sarcoplasmic reticulum in situ is an intricate tubular network that surrounds the contractile material in striated muscle cells. Its topographical relationship to other intracellular components, especially the myofibrils, is rather rigidly mainiained by a cytoskeleton which enmeshes Z line material and sarcoplasmic reticulum and, ultimately, is anchored at the plasmalemma. As a result, the two main components of the sarcoplasmic reticulum, the junctional SR and the free SR, retain their typical location in the A band region and in the I band region, respectively. The junc­tional SR, which is thought to be the site for calcium storage and release for contraction, is, thus, always well within one micron of the regulatory proteins associated with the actin filaments. The junctional SR, a synonym for terminal cisterna applying to both skeletal and cardiac muscle, is generally held to be involved in the translation of the action potential into calcium release, mainly because of the close topographic apposition between the junctional SR and the plasmalemma, especially in skeletal muscle. This attractive structure-function correlation is challenged by the observation that in bird cardiac muscle 80% of the junctional SR is spacially far removed from plas­malemma, the site of electrical activity. This anomalous topography is not in conflict with the notion that translation of the action potential into calcium release may be accomplished by a dif­fusible transmitter substance, e.g. calcium. Any hypothesis dealing with this problem must ac­ count for the anatomy of the bird heart.

scholarly journals The Builders of the Junction: Roles of Junctophilin1 and Junctophilin2 in the Assembly of the Sarcoplasmic Reticulum–Plasma Membrane Junctions in Striated Muscle

Biomolecules ◽  
2022 ◽  
Vol 12 (1) ◽  
pp. 109
Author(s):  
Stefano Perni
Keyword(s):  
Plasma Membrane ◽  
Sarcoplasmic Reticulum ◽  
Intracellular Calcium ◽  
Cardiac Muscle ◽  
Structure Prediction ◽  
Calcium Release ◽  
Striated Muscle ◽  
Short Review ◽  
Published Data ◽  
Intracellular Calcium Release

Contraction of striated muscle is triggered by a massive release of calcium from the sarcoplasmic reticulum (SR) into the cytoplasm. This intracellular calcium release is initiated by membrane depolarization, which is sensed by voltage-gated calcium channels CaV1.1 (in skeletal muscle) and CaV1.2 (in cardiac muscle) in the plasma membrane (PM), which in turn activate the calcium-releasing channel ryanodine receptor (RyR) embedded in the SR membrane. This cross-communication between channels in the PM and in the SR happens at specialized regions, the SR-PM junctions, where these two compartments come in close proximity. Junctophilin1 and Junctophilin2 are responsible for the formation and stabilization of SR-PM junctions in striated muscle and actively participate in the recruitment of the two essential players in intracellular calcium release, CaV and RyR. This short review focuses on the roles of junctophilins1 and 2 in the formation and organization of SR-PM junctions in skeletal and cardiac muscle and on the functional consequences of the absence or malfunction of these proteins in striated muscle in light of recently published data and recent advancements in protein structure prediction.

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