Mechanisms underlying the genesis of post-rest contractions in cardiac muscle

1. Post-rest potentiation reflects basic cellular mechanisms that control cardiac muscle contraction. Transmembrane calcium influx, the Na+/Ca2+ exchange and the function of intracellular stores that liberate activator calcium upon activation are some of the mechanisms involved. 2. Three aspects of the post-rest potentiated phenomenon were investigated, using isometrically contracting rat papillary muscles and toad ventricle strips: dependence on 1) inotropic state of steady-state contractions, 2) pause duration and Na+/Ca2+ exchange activity, and 3) the extent of transmembrane calcium influx. 3. The results suggest that the potentiated state of post-rest contractions increases linearly with the inotropic state of preceding steady-state control contractions. As the pause duration increases from 5 to 240 s, the post-rest potentiation also increases, attaining a steady level after 30-s pauses. During the pause, the Na+/Ca2+ exchange mechanism operates at an activity level that can alter the amount of activator calcium used for post-rest contractions. Interventions that increase intracellular Na+, such as the increase of the stimulation rate from 0.5 to 1 Hz or the increase of extracellular NaCl concentration to 160 mM, reduce the Na+/Ca2+ activity, increasing intracellular Ca2+ and post-rest potentiation. The decrease of transmembrane Ca2+ influx during activation increases the relative participation of the sarcoplasmic reticulum in the development of post-rest potentiation. Reduction of extracellular Ca2+ concentration from 1.25 mM to 0.25 mM or the use of 1 microM verapamil and 2 mM manganese increases the relative potentiation of post-rest contractions. This is particularly observed in toad ventricle strips since post-rest potentiation, which does not develop under control conditions, is observed after verapamil or manganese treatment. The results suggest that the excitation-contraction coupling process operating for post-rest contraction activation, unlike that operating for steady-state contraction activation, depends more on the calcium stored at intracellular sites than on transmembrane calcium influx.