Caffeine induces muscle contracture by acting on the outer surface of the muscle membrane without altering membrane potential, suggesting a non-electrical mechanism linking the membrane to contractile elements.
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No immediate clinical translation from this animal model; hypothesis-generating for non-electrogenic membrane-contractile coupling.
Summary. When a frog's striated muscle (m. sartorius) is immersed in Ringer solution containing 2.5–10 × 10– 4 w/v of the free base caffeine tension develops and the muscle contracts. The contracture is graded according to dose and reverses rapidly upon removal of the drug. Higher concentrations of caffeine produce an irreversible contracture. In a muscle immersed in isotonic K 2 SO 4 or KCl solution caffeine produces exactly the same kind of muscle contracture as in a muscle kept in Ringer's fluid. Prolonged soaking (96 hours) of a muscle in isotonic K 2 SO 4 solution does not reduce its responsiveness to caffeine. Local application of caffeine from a micropipette to a muscle fibre produces a localized contracture when the tip of the pipette is at the outer surface of the cell membrane. When the tip is inserted into the fibre no contracture is observed indicating that the caffeine action is confined to the muscle membrane. In concentrations helow 10 ‐3 w/v caffeine does not alter the resting meinhrane potential of iituscle fibres. Neither does the drug markedly reduce the transverse niuscle iiienibraiie resistance. It is suggested that caffeine at the niuscle membrane starts a process which activates the contractile mechanism in the interior of the fibre. This process is believed to be the same as that activated by the propagated action potential. The nature of the process (or processes) linking the membrane to the contractile elements is unknown hut the present results makes it unlikely that it is an electric current or potential change.
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Axelsson et al. (1958) studied this question.
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