Abstract
When cardiac muscle shortens during a contraction, the duration of mechanical activity is abbreviated (shortening deactivation), but the duration of the action potential is prolonged. Neither of these phenomena is fully understood, but both may be related to changes in the myoplasmic free calcium concentration. In these experiments, isolated papillary muscles from cats and ferrets were allowed to contract under various mechanical conditions while myoplasmic calcium was monitored with aequorin, or in parallel experiments the membrane potential was recorded with microelectrodes or a sucrose gap. When shortening occurred, myoplasmic calcium was increased and the membrane potential was more positive than in isometric contractions. The changes in calcium apparently precede the depolarization. We propose that muscle shortening reduces calcium binding to the contractile proteins and leads to a rise in myoplasmic calcium, and that this rise in myoplasmic calcium activates an inward current leading to the observed changes in the action potential. These processes may be important contributory factors in some arrhythmias.
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