[Effects of caffeine on post-extrasystolic potentiation and mechanical restitution in mammalian papillary muscle].

The excitation-contraction coupling theory postulates that the main source of activator calcium is the sarcoplasmic reticulum that releases calcium in response to an electrical stimulus. This happens to be true in skeletal muscle, but recently several discrepancies have been raised about the validity of this hypothesis in cardiac muscle. These discrepancies are related to morphological as well as physiological data. The new information postulates that sarcoplasmic reticulum in cardiac muscle does not supply calcium as a main source in physiological conditions. The aim of the present paper was to evaluate the sarcoplasmic reticulum role in the supply of activator calcium in excitation-contraction coupling. A series of experiments were performed using the mechanical restitution and the post-extrasystolic potentiation models in the presence of caffeine, which is known to provoke functional elimination of the sarcoplasmic reticulum. It was observed that caffeine diminished the post-extrasystolic potentiation when 1 mM was used. At higher dose (4mM) the post-extrasystolic potentiation was completely abolished. On the other hand the late part of mechanical restitution is also abolished by caffeine. The amount of calcium that recirculates seems to increase in the presence of caffeine. The results obtained seem to support the idea that the sarcoplasmic reticulum has only a minor role in the supply of activator calcium, when physiological stimulation rates are used.