Two sources of calcium contribute to the rise in cytoso-lic calcium that initiates smooth-muscle contraction: (1) the sarcoplasmic reticulum and (2) extracellular calcium entering the cell through plasma-membrane calcium channels. The amount of calcium contributed by these two sources differs among various smooth muscles, some being more dependent on extracellular calcium than the stores in the sarcoplasmic reticulum, and vice versa.
Let us look first at the sarcoplasmic reticulum. The total quantity of this organelle in smooth muscle is smaller than in skeletal muscle, and it is not arranged in any specific pattern in relation to the thick and thin filaments. Moreover, there are no T tubules connected to the plasma membrane in smooth muscle. The small fiber diameter and the slow rate of contraction do not require such a rapid mechanism for getting an excitatory signal into the muscle fiber. Portions of the sar-coplasmic reticulum are located near the plasma membrane, however, forming associations similar to the relationship between T tubules and the lateral sacs in skeletal muscle. Action potentials in the plasma membrane can be coupled to the release of sarcoplasmic-reticulum calcium at these sites. In addition, second messengers released from the plasma membrane or generated in the cytosol in response to the binding of extracellular chemical messengers to plasma-membrane receptors, can trigger the release of calcium from the more centrally located sarcoplasmic reticulum.
What about extracellular calcium in excitation-contraction coupling? There are voltage-sensitive calcium
PART TWO Biological Control Systems
PART TWO Biological Control Systems channels in the plasma membranes of smooth-muscle cells, as well as calcium channels controlled by extracellular chemical messengers. Since the concentration of calcium in the extracellular fluid is 10,000 times greater than in the cytosol, the opening of calcium channels in the plasma membrane results in an increased flow of calcium into the cell. Because of the small cell size, the entering calcium does not have far to diffuse to reach binding sites within the cell.
Removal of calcium from the cytosol to bring about relaxation is achieved by the active transport of calcium back into the sarcoplasmic reticulum as well as out of the cell across the plasma membrane. The rate of calcium removal in smooth muscle is much slower than in skeletal muscle, with the result that a single twitch lasts several seconds in smooth muscle but lasts only a fraction of a second in skeletal muscle.
Moreover, whereas in skeletal muscle a single action potential releases sufficient calcium to turn on all the cross bridges in a fiber, only a portion of the cross bridges are activated in a smooth-muscle fiber in response to most stimuli. Therefore, the tension generated by a smooth-muscle fiber can be graded by varying cytosolic calcium concentration. The greater the increase in calcium concentration, the greater the number of cross bridges activated, and the greater the tension.
In some smooth muscles, the cytosolic calcium concentration is sufficient to maintain a low level of cross-bridge activity in the absence of external stimuli. This activity is known as smooth-muscle tone. Its intensity can be varied by factors that alter the cytosolic calcium concentration.
As in our description of skeletal muscle, we have approached the question of excitation-contraction coupling in smooth muscle backward by first describing the coupling (the changes in cytosolic calcium), and now we must ask what constitutes the excitation that elicits these changes in calcium concentration.
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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.