RESUMO
Post-rest potentiation reflects basic cellular mechanisms that control cardiac muscle contraction. Transmembrane calcium influx, the Na+/Ca*+ exchange and the function of intracellular stores that liberate activator calcium upon activation are some of the mechanisms involved. 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+/Ca*+ exchange activity, and 3) the extent of transmembrane calcium influx. 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+/Ca*+ 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 extracxellular NaCl concentration to 160 mM, reduce the Na+/Ca*+ activity, increasing intracellular Ca*+ and post-rest potentiation. The decrease of transmembrane Ca*+ and post-rest potentiation. The decrease of transmembrane Ca*+ influx during activation increases the relative participation of the sarcoplasmic reticulum in the development of post-r5est potentiation. Reduction of extracellular Ca*+ concentration from 1.25 mM to 0.25 mM or the use of 1 uM verapamil and 2 mM manganese increases the relative potentiation of post-rest contractions. This is particulary 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