Publisher Summary Ca release from the sarcoplasmic reticulum (SR) is one of the most important steps in excitation–contraction coupling of skeletal muscle. This chapter describes the physiological release of Ca from the SR, various modes of Ca release from the SR, and the physiological significance of various Ca release mechanisms. Ca ion is the mediator of information of action potentials to the contractile machinery; however, the physiological source of the mediator Ca is not yet unequivocally established. The inhibitors of Ca-induced Ca release––procaine and adenine––were shown not to inhibit contraction of living skeletal muscle fibers induced by the depolarization of the surface membrane. Studies of the ionic composition of the lumen of the SR by electron-probe analysis show that there are no significant differences between the ionic compositions in the lumen of the SR and that in the cytoplasm except for Ca ion. The essential part of the physiological Ca release mechanism is almost entirely unknown; therefore, further studies, especially by using preparations, such as improved cut fibers, that retain the physiological tubule (T)–SR coupling mechanism, but have easy access to sarcoplasm so that its composition can be altered at will, are necessary.

Calcium release from the sarcoplasmic reticulum

Caffeine and the central nervous system: mechanisms of action, biochemical, metabolic and psychostimulant effects.

(1974). Actin And Myosin And Cell Movemen. CRC Critical Reviews in Biochemistry: Vol. 2, No. 1, pp. 1-65.

Actin and myosin and cell movement.

The repeated contractions which can be observed in skinned fibres in appropriate concentrations of caffeine, Ca2+ and chelating agent suggest that calcium release is a regenerative process in which calcium itself causes the release of calcium from the reticulum.

Calcium induced release of calcium from the sarcoplasmic reticulum of skinned skeletal muscle fibres.

As is well known, the memorable discovery of Galvani (1791) was followed by the development of two new fields of science, electrochemistry and electrophysiology. During the course of this development, the most remarkable feature of the original finding, i.e. ‘contraction of muscle induced by a piece of metal’, gradually came to be ignored. As a consequence, the simple question as to how electrical stimulation might induce muscle contraction was left unanswered until the middle of this century, when several physiologists became aware of the crucial nature of the problem and tried to attack it from various directions. This resulted in a marked progress of physiological and morphological studies which were intentionally or unintentionally concerned with the mechanism of the link between excitation, that is the electrical phenomenon at the surface membrane, and the contractile process.

https://www.cambridge.org/core/services/aop-cambridge-core/content/view/S0033583500001190

Control of muscle contraction

At concentrations between 1 to 10 mM, caffeine reduced the Ca-accumulating capacity of fragmented reticulum obtained from frog and rabbit muscle. With 8 mM caffeine enough Ca was released from frog reticulum to account for the force of the contracture. Caffeine did not affect all reticulum membranes equally. The fraction which was spun down at 2000 g was more sensitive than the lighter fractions. The percentage of the total accumulated Ca released by caffeine decreased with decreasing Ca content of the reticulum. In parallel with their known effects on the caffeine contracture, a drop in temperature increased the caffeine-induced Ca release while procaine inhibited it. Caffeine also inhibited the rate of Ca uptake, which may in part account for the prolongation of the active state caused by caffeine.

https://rupress.org/jgp/article-pdf/52/5/750/1244348/750.pdf

R Herz

Papers

The Relationship between Caffeine Contracture of Intact Muscle and the Effect of Caffeine on Reticulum