Abstract

Intracellular action potentials and peak force (F) of isometric contractions were recorded from ventricular trabeculae of adult rats at 26 degrees C. The duration of the action potentials was measured at 50% of the amplitude (APD50) and at 10% of the amplitude (APD10). The effect of a variety of experimental interventions on the three variables was studied. APD50 reflects the duration of the plateau phase which is typically about 30 ms in rat myocardium. APD10 reflects the sum of the duration of the plateau phase and of the slow final repolarization phase (phase 3') and is about 80 ms. During paired-pulse stimulation, strong contractions coincided with shortened APD50 and prolonged APD10, i.e. a negative APD50-F and a positive APD10-F relationship was obtained. Addition of Sr2+ to the medium caused an increase of F and prolongation of APD50 and APD10. Nifedipine caused a decrease of F and a shortening of APD50 and APD10. Substitution of extracellular NaCl by LiCl caused an increase of F but a shortening of APD50 and APD10. An increase of [Ca2+]o caused an increase of F whereas APD50 was almost constant and APD10 increased. A simple model is proposed which explains the results, assuming that: the effect of paired-pulse stimulation is related to time dependent intracellular Ca2+ transport; Sr2+ and nifedipine act mainly on isi; NaCl substitution inhibits Na+/Ca2+ exchange; and [Ca2+]o affects both isi and Na+/Ca2+ exchange.

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