Springer Online Journal Archives 1860-2000
Summary 1. In isolated guinea-pig papillary muscles, noradrenaline (10−7–10−4 M) augmented the peak force of contraction after rest periods of 10–15 min (rested-state contractions) to the same extent as during continued stimulation at rates of 0.2–1 Hz. However, there were great differences in the shape of the isometric contraction curves dependent upon the two experimental conditions. 2. The rested-state contractions developed with a latency of about 100 ms and reached peak force more than 200 ms after the stimulus. Noradrenaline increased this late contraction manyfold without a shortening of the latency period. 3. In addition to the late contraction peak, an early contraction component developed at 0.2 Hz frequency. It reached its maximal force within the first 100 ms after the stimulus. Noradrenaline, in the same concentration range, increased the force and steepness of the early component of contraction to about the same extent as of the late component, i.e., the rested-state contraction. 4. Increasing the frequency of contraction up to 1 Hz augmented the early component of contraction and diminished the late component, concomitantly with a shortening of the action potential and the total contraction time. 5. In regard to the influence on the two components of contraction, dibutyryl-cyclic-adenosine-monophosphate (1–4 mM) resembled that of noradrenaline. 6. In contrast to the rested-state contractions as influenced by noradrenaline or dibutyryl-cyclic-AMP, rested-state contractions, increased either by a high concentration (2×10−4 M) of dihydro-ouabain or by a reduction of the external sodium concentration (to 40 mM), showed a steep rise early after the stimulus and reached peak force within 125 ms. 7. It is concluded that, in the resting muscle, noradrenaline augments Ca accumulation by a cellular store (store II), probably the sarcoplasmic reticulum. Ca ions, released from this store with a latency during a long lasting action potential, cause the late appearing rested-state contraction. After its release, part of the Ca may be bound by another store (store I, located probably at the sarcolemma); from this it is set free during subsequent excitations, thereby causing an additional early component of contraction.
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