the region of the T tubules and immediately adjacent sarcoplasmic reticulum. (2) This small increase in calcium concentration then causes calcium to bind to calcium receptors on the external surface of the sar-coplasmic reticulum membranes. (3) These calcium-sensitive receptors contain intrinsic calcium channels, and activation of the receptors opens the channels, allowing a large net diffusion of calcium from the calcium-rich interior of the sarcoplasmic reticulum into the cytosol (this is termed "calcium-induced calcium release"). (4) It is mainly this calcium that causes the contraction.
Thus, even though most of the calcium causing contraction comes from the sarcoplasmic reticulum, the process—unlike that in skeletal muscle—is dependent on the movement of extracellular calcium into the muscle, the calcium then acting as the signal for release of the sarcoplasmic-reticulum calcium.
Contraction ends when the cytosolic calcium concentration is restored to its original extremely low value by active transport of calcium back into the sarcoplasmic reticulum. Also, an amount of calcium equal to the small amount that had entered the cell from the extracellular fluid during excitation is transported out of the cell, so that the total cellular calcium content remains constant. (The transport mechanisms involved in these movements offer an excellent review of key aspects of calcium transport described in Chapter 6. The transport into the sarcoplasmic reticulum is by primary active Ca-ATPase pumps; the transport across the plasma membrane is also by Ca-ATPase pumps plus Ca/Na exchangers.)
As we shall see, how much cytosolic calcium concentration increases during excitation is a major determinant of the strength of cardiac-muscle contraction. In this regard, cardiac muscle differs importantly from skeletal muscle, in which the increase in cyto-solic calcium occurring during membrane excitation is always adequate to produce maximal "turning-on" of cross bridges by calcium binding to all troponin sites. In cardiac muscle, the amount of calcium released from the sarcoplasmic reticulum is not usually sufficient to saturate all troponin sites. Therefore, the number of active cross bridges and thus the strength of contraction can be increased still further if more calcium is released from the sarcoplasmic reticulum.
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This ebook provides an introductory explanation of the workings of the human body, with an effort to draw connections between the body systems and explain their interdependencies. A framework for the book is homeostasis and how the body maintains balance within each system. This is intended as a first introduction to physiology for a college-level course.