Ryanodine receptors calcium release

Fill M, Copello JA (2002) Ryanodine receptor calcium release channels. Physiol Rev 82 893-922... 

Malignant hyperthermia caused by mutant ryanodine receptor calcium release channels 723... 

Bidasee, K. R., Nallani, K., Yu, Y., Cocklin, R. R., Zhang, Y., Wang, M., Dincer, U. D., and Besch, H. R., Jr. (2003b). Chronic Diabetes Increases Advanced Glycation end Products on Cardiac Ryanodine Receptors/Calcium-Release Channels. Diabetes 52(7) 1825-36. 

Ma, J., Hayek, S. M., and Bhat, M. B. (2004). Membrane Topology and Membrane Retention of the Ryanodine Receptor Calcium Release Channel. Cell Biochem Biophys 40(2) 207-24. 

Marks, A. R. (2001). Ryanodine Receptors/Calcium Release Channels in Heart Failure and Sudden Cardiac Death. . / Mol Cell Cardiol 33(4) 615-24. 

Scoote, M., and Williams, A. J. (2002). The Cardiac Ryanodine Receptor (Calcium Release Channel) Emerging Role in Heart Failure and Arrhythmia Pathogenesis. Cardiovasc Res 56(3) 359-72. 

Terentyev, D., Nori, A., Santoro, M., Viatchenko-Karpinski, S., Kubalova, Z., Gyorke, I., Terentyeva, R., Vedamoorthyrao, S., Blom, N. A., Valle, G., Napolitano, C., Williams, S. C., Volpe, P., Priori, S. G., and Gyorke, S. (2006). Abnormal Interactions of Calsequestrin with the Ryanodine Receptor Calcium Release Channel Complex Linked to Exercise-Induced Sudden Cardiac Death. Circ Res 98(9) 1151-8. 

Tester, D. J., Carturan, E., Dura, M., Reiken, S., Wronska, A., Marks, A. R., and Ackerman, M. J. (2006b). Molecular and Functional Characterization of Novel RyR2-Encoded Cardiac Ryanodine Receptor/Calcium Release Channel Mutations in Sudden Infant Death Syndrome. Heart Rhythm 3(5-Sl) S67. 

Marks, A. R. 2001. Ryanodine receptors/calcium release channels in heart failure and sudden cardiac death. J. Mol. Cell. Cardiol. 33 615-624. 

Dulhunty A, Gage P et al (2001) The glutathione transferase structural family includes a nuclear chloride channel and a ryanodine receptor calcium release channel modulator. J Biol Chem 276 3319-3323... 

A recent paper from Iwata et al. (2003) described a channel of the TRP family which is activated in response to growth factors or stretch, and whose activity is elevated in dystrophic skeletal and cardiac muscle. Under normal conditions, the GRC is located on vesicles in the cytoplasm, but translocates to the sarcolemma in response to growth factor signaling or stretch. This translocation is calcium-dependent, and, interestingly, requires a Gd3+-sensitive conductance, which could represent a basal level of GRC activity or some other perhaps MS-type channel. In addition, the translocation is inhibited by ruthenium red, a blocker of ryanodine receptor-dependent release of SR calcium, suggesting that store calcium release is also necessary for sarcolemmal GRC insertion. Whether the GRC is an SOC was not reported. 

The L-type VDCC plays a critical role in excitation-contraction coupling, as voltage activation of VDCC results in activation of ryanodine receptors and release of calcium from the SR. Studies of VDCC in dystrophic muscle have produced... 

Dantrolene is a hydantoin class of anticonvulsant that acts outside the central nervous system to produce skeletal muscle relaxation by interfering with excitation contraction coupling. In normally contracting muscle, activation of the ryanodine receptor within the muscle fiber results in calcium release from the sarcoplasmic reticulum and subsequent muscle contraction. Dantrolene interferes with the release of calcium from the sarcoplasmic reticulum by interfering with the ryanodine receptor. The release of calcium in smooth and cardiac muscle is under different control consequently, dantrolene primarily affects skeletal muscle. 

Fig. 47.3. Events leading to sarcoplasmic reticulum calcium release in skeletal muscle. 1. Acetylcholine, released at the synaptic cleft, binds to acetylcholine receptors on the sar-colemma, leading to a change of conformation of the receptors such that they now act as an ion pore. This allows sodium to enter the cell and potassium to leave. 2. The membrane polarization that results from these ion movements is transmitted throughout the muscle fiber by the T-tubule system. 3. A receptor in the T-tubules (the dihydropyridine receptor, DHPR) is activated by membrane polarization (a voltage-gated activation) such that activated DHPR physically binds to and activates the ryanodine receptor in the sarcoplasmic reticulum (depolarization-induced calcium release). 4. The activation of the ryanodine receptor, which is a calcium channel, leads to calcium release from the SR into the sarcoplasm. In cardiac muscle, activation of DHPR leads to calcium release from the T-tubules, and this small calcium release is responsible for the activation of the cardiac ryanodine receptor (calcium-induced calcium release) to release large amounts of calcium into the sarcoplasm.

The open probability of ryanodine-sensitive calcium release channels in cardiac and smooth muscle increases with cytoplasmic calcium, and this property of the ryanodine receptor has been referred to as calcium-in-... 

Calsequestrin is the major calcium storage protein of the sarcoplasmic reticulum in skeletal and cardiac muscles. It is highly acidic and has a large capacity for Ca2+. Calsequestrin functions to localize calcium near the junctional face of the terminal cistemae from which calcium can be released into the cytosol via the ryanodine receptor. 

Calcium couples muscle membrane excitation to filament contraction. Important work has focused on the proteins present in the T-tubule/SR junction. One protein, an integral component of the T-tubular membrane, is a form of L-type, dihydropyridine-sensitive, voltage-dependent calcium channel. Another, the ryanodine receptor (RyR), is a large protein associated with the SR membrane in the triad that may couple the conformational changes in the Ca2+ channel protein induced by T-tubular depolarization to the Ca2+ release from the SR (Fig. 43-6). 

The first molecule, the Ca2+ channel, is required for coupling at the triad. Skeletal muscle contains higher concentrations of this L-type Ca2+ channel that can be accounted for on the basis of measured voltage-dependent Ca2+ influx because much of the Ca2+ channel protein in the T-tubular membrane does not actively gate calcium ion movement but, rather, acts as a voltage transducer that links depolarization of the T-tubular membrane to Ca2+ release through a receptor protein in the SR membrane. The ryanodine receptor mediates sarcoplasmic reticulum Ca2+ release. The bar-like structures that connect the terminal elements of the SR with the T-tubular membrane in the triad are formed by a large protein that is the principal pathway for Ca2+ release from the SR. This protein, which binds the... 

Calcium release by ryanodine receptors in smooth muscle... 

Marx SO, Reiken S, Hisamatsu Y et al 2000 PKA phosphorylation dissociates FKBP12.6 from the calcium release channel (ryanodine receptor) defective regulation in failing hearts. Cell 101 365-376... 

Ryanodine receptor- and IP3 receptor-mediated calcium release from the sarcoplasmic reticulum. 

---