Contraction coupling, in heart

Cheng H, Lederer WJ, Cannell MB 1993 Calcium sparks elementary events underlying excitation—contraction coupling in heart muscle. Science 262 740—744 Collier ML, Thomas AP, Berlin JR 1999 Relationship between L-type Ca2+ current and unitary sarcoplasmic reticulum Ca2+ release events in rat ventricular myocytes. J Physiol (Lond)... 

Cheng H, Lederer WJ, Cannell MB 1993 Calcium sparks elementary events underlying excitation-contraction coupling in heart muscle. Science 262 740—744... 

Figure 6.4. Exitation contraction coupling in heart muscle. Influx of extracellular Ca through the voltage-gated anesthetics receptor opens the ryanodine receptor in the sarcoplasmic reticulum (SR), which releases the bulk of Ca required for myofll-ament activation. Opening of lyanodine receptors by Ca will spread like a wave along the SR membrane - a kind of chemical membrane excitation.

Farrell, E.F., Antaramian, A., Rueda, A., et al., 2003, Sorcin inhibits calcium release and modulates excitation-contraction coupling in the heart. J Biol Chem, 278, pp 34660-66. 

Hobai, I.A., O Rourke, B. 2001, Decreased sarcoplasmic reticulum calcium content is responsible for defective excitation-contraction coupling in canine heart failure. Circulation, 103(11), pp 1577-84. 

It is well documented that coordinated myocyte handling of Ca2+ is essential for efficient excitation-contraction coupling in the heart. Since cardiac pump is able to alter its function in response to any requirement in the body and the regulation of contractile function of individual myocytes obtained by modulation of intracellular Ca2+ signaling, the characteristics of regulation induced by adrenergic stimulations are very important for maintaining the normal heart function in humans. 

Figure 6.6. Excitation contraction coupling in skeletal muscle (a, b) and heart muscle (c). In skeletal muscle, the anesthetics receptor (DHPR) and the ryanodine receptor (RyR) are in direct contact (a). The conformational change to the former that occurs in response to membrane depolarization is sufficient to induce Ca release from the SR a flow of Ca across the plasma membrane is not necessary (b). In heart muscle, however, this direct link does not exist, and Ca must therefore enter through the DHPR first (c).

Fleckenstein, A. Specific inhibitors and promoters of calcium action in the excitation-contraction coupling of heart muscle. Tn Calcium and the Heart, eds. Harris, P and Opie, L. Academic Press, London 1970, 135-188. 

Sorcin (soluble resistance-related calcium binding protein) was isolated from multidrug-resistant cells and is expressed in a few mammalian tissues such as skeletal muscle, heart, and brain. In the heart, sorcin interacts with the ryanodine receptor and L-type Ca2+-channels regulating excitation in contraction coupling. 

Modern representations of the virtual heart, therefore, describe structural aspects like fibre orientation in cardiac muscle, together with the distribution of various cell types, active and passive electrical and mechanical properties, as well as the coupling between cells. This then allows accurate reproduction of the spread of the electrical wave, subsequent contraction of the heart, and effects on blood pressure, coronary perfusion, etc. It is important to point out, here, that all these parameters are closely interrelated, and changes in any one of them influence the behaviour of all others. This makes for an exceedingly complex system. 

Actin, role in heart excitation and contraction coupling, 5 81 Actinide carbides, 4 689 Actinide carbonate, 25 430-431 Actinide-gallium compounds, 22 355 Actinide oxides, 24 761 Actinide peroxides, 28 410 Actinides, 23 569. See also Actinides and transactinides Actinide series absorption and fluorescence spectra, 2 490... 

Myocardial infarction, 3 710-711 and blood coagulation, 4 81 Myocardial pacemaker cells, 5 81 Myocardium, 5 79—80 Myoglobin, properties of standard, 3 836t Myosin, role in heart excitation and contraction coupling, 5 81 Myrac aldehyde, 2 278 24 485 Myrascone, 24 571... 

Vatner, D.E., Sato, N., Kiuchi, K., et al., 1994, Decrease in myocardial ryanodine receptors and altered excitation-contraction coupling early in the development of heart failure. Circulation, 90(3), pp 1423-30. 

Although it is believed that the primary defect in early heart failure resides in the excitation-contraction coupling machinery of the heart, the clinical condition also involves many other processes and organs, including the baroreceptor reflex, the sympathetic nervous system, the kidneys, angiotensin II and other peptides, and death of cardiac cells. Recognition of these factors has resulted in evolution of a variety of treatment strategies (Table 13-1). 

Nearly all cells in the body exhibit a difference in electrical voltage between their interior and exterior, the membrane potential. Some cells, including the conducting and contracting cells of the heart, are excitable an appropriate stimulus alters the properties of the cell membrane, ions flow across it and elicit an action potential. This spreads to adjacent cells, i.e. it is conducted as an electrical impulse and, when it reaches a muscle cell, causes it to contract this is excitation-contraction coupling. 

Bristow M, Ginsburg R, Umans V, et al. pr and p2-adrenergic-receptor subpopulations in nonfailing and failing human ventricular myocardium coupling of both receptor subtypes to muscle contraction and selective Pj -receptor down-regulation in heart failure. Circ Res 1986 59 297-309. 

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