scholarly journals The Ca2+-Induced Structural Changes in Troponin In-Situ and In-Vitro: A FRET Study in Permeabilized Cardiac Muscle Fibers and Reconstituted Thin Filaments

2013 ◽  
Vol 104 (2) ◽  
pp. 482a
Author(s):  
King-Lun Li ◽  
John R. Solaro ◽  
Wenji Dong
1998 ◽  
Vol 78 (2) ◽  
pp. 359-391 ◽  
Author(s):  
BARRY M. MILLMAN

Millman, Barry M. The Filament Lattice of Striated Muscle. Physiol. Rev. 78: 359–391, 1998. — The filament lattice of striated muscle is an overlapping hexagonal array of thick and thin filaments within which muscle contraction takes place. Its structure can be studied by electron microscopy or X-ray diffraction. With the latter technique, structural changes can be monitored during contraction and other physiological conditions. The lattice of intact muscle fibers can change size through osmotic swelling or shrinking or by changing the sarcomere length of the muscle. Similarly, muscle fibers that have been chemically or mechanically skinned can be compressed with bathing solutions containing very large inert polymeric molecules. The effects of lattice change on muscle contraction in vertebrate skeletal and cardiac muscle and in invertebrate striated muscle are reviewed. The force developed, the speed of shortening, and stiffness are compared with structural changes occurring within the lattice. Radial forces between the filaments in the lattice, which can include electrostatic, Van der Waals, entropic, structural, and cross bridge, are assessed for their contributions to lattice stability and to the contraction process.


2000 ◽  
Vol 276 (7) ◽  
pp. 5353-5359 ◽  
Author(s):  
Christian C. Witt ◽  
Brenda Gerull ◽  
Michael J. Davies ◽  
Thomas Centner ◽  
Wolfgang A. Linke ◽  
...  

1962 ◽  
Vol 202 (5) ◽  
pp. 905-908 ◽  
Author(s):  
Louis Tobian ◽  
Jeanette Janecek ◽  
John Foker ◽  
Dorothy Ferreira

Administration of chlorothiazide to rats for 9 weeks produces an increase of intracellular sodium and a decrease of intracellular potassium in skeletal muscle. However, in cardiac muscle, in the wall of mesenteric arterioles, in aortic wall, and in kidney there is no significant alteration in the amount of sodium, potassium, or chloride per unit of dry tissue weight. The water content of heart muscle, skeletal muscle, and kidney is not altered by chlorothiazide. The intracellular concentration of Na and K in heart muscle is likewise unaltered by chlorothiazide. However, chlorothiazide produces a highly significant 44% increase in the granularity of the juxtaglomerular cells. The data in general suggest that chlorothiazide decreases the volume of extracellular fluid, but does not reduce the content of intracellular Na. Extracellular K is reduced as well as the K inside skeletal muscle fibers. However, the amount of K inside cardiac muscle fibers is unchanged by chlorothiazide.


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