We tested Shattock and Bers' (1989) hypothesis according to which in rat cardiac myocytes net Ca2+ influx during diastole via Na/Ca exchange provides the main route of entry of Ca2+ available for activation of contractions. We used injections of caffeine into the close vicinity of the single, isolated rat or guinea-pig ventricular myocytes in order to release Ca2+ from sarcoplasmic reticulum (SR). The cells responded to caffeine with a transient contracture, the amplitude of which was regarded as a relative index of SR Ca2+ content. Application of caffeine deprived the SR of Ca2+. This was manifested by a very small (rat) or absent (guinea-pig) contractile response to the second application of caffeine and by a decrease of the amplitude of the first post caffeine contraction to 8 +/- 3% (rat) or to 16 +/- 6% (guinea-pig) of control. In the rat myocytes SR deprived of Ca2+ was able to recover its Ca2+ store even in the resting cell. This was indicated by the time dependent recovery of contractile response to the second application of caffeine and of the amplitude of the post-caffeine electrically evoked contractions. The recovery of post-caffeine contractile responses was completely inhibited by Ca2+ free solution, by 5.0 mM Ni+ and by low K+ (1.0 mM) hyperpolarising solution superfused from the first application of caffeine or during rest. The recovery was enhanced by superfusion of the cells with low Na+ (50%) solution. These results show that there is a considerable net Ca2+ influx by means of Na/Ca exchange and then the SR Ca2+ uptake in the resting rat myocytes.(ABSTRACT TRUNCATED AT 250 WORDS)

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http://dx.doi.org/10.1016/0022-2828(90)90059-bDOI Listing

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