Inhibition of the slow response action potential during the aftercontraction in mammalian heart muscle

Abstract

In experiments on isolated guinea-pig papillary muscles the excitability of the cellular membrane was investigated during the aftercontractions (ACs) induced by lowering the perfusate temperature to 15°C, addition of noradrenaline (10 −5 m) and raising CaCl 2 to 15 m m. No changes in membrane potential were observed during ACs. At stimulation rate of 0.2 Hz the amplitude of the first AC was 21 ± 3% ( n = 6) of the main twitch and the peak of this AC appeared after the peak of the main twitch with delay of 1.6 ± 0.2 s. The recovery process for maximal upstroke rate of action potential and the strength-interval curve were shown to proceed without any transients during AC. This indicates that an increase of intracellular Ca 2+ concentration during AC has no effects on the fast Na + channel activity. The slow response action potentials recorded in the high K + (25 m m) were decreased significantly during AC. The reduction of slow response amplitude during AC could not be explained by the increase of threshold only because even at supramaximal intensity of stimulation this reduction was still visible and equal to 22 ± 1 mV. It was concluded that a slow channel activity of cardiac membrane might depend on the intracellular Ca 2+ concentration and thereby be determined by the efficiency of Ca 2+ sequestering systems in the cell. Caffeine (2 m m) abolished the ACs. After-releases of Ca 2+ from sarcoplasmic reticulum were suggested as the causes of these ACs.