Key result
Caffeine (10 mm) rapidly released calcium pool A and decreased its steady state by 60%, while procaine (5 mm) inhibited caffeine-triggered release by 50% in the perfused rat heart.
The study provides evidence that cellular calcium pool A is located in the sarcoplasmic reticulum and its release to myofibrils is triggered by excitation-dependent calcium influx.
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Hypothesis-generating for SR calcium release mechanisms; leaves open translation to human excitation-contraction coupling.
Pool A is a rapidly exchangeable cellular pool of Ca++ whose release is triggered by a mechanism involving extracellular Ca++ (Hunter et al., 1981). We have now found that pool A is rapidly released from the perfused rat heart when 10 mm caffeine is added to the perfusate. Pool A release by caffeine was demonstrated during a Ca++ free perfusion. When the perfusate contained 2.5 mm Ca++, caffeine induced an immediate contractile failure. The steady state level of pool A (normally 69 +/- 10 nmol Ca++/g wet wt heart) was also decreased by 60%. Pool A was similarly depleted in hearts perfused with medium containing 0.2 mm Ca++. Procaine (5 mm) inhibited by 50% the release of pool A triggered by caffeine and inhibited by 86% the release triggered by extracellular Ca++. The inhibition of Ca++-induced release of pool A by procaine was partially relieved by externally stimulating the hearts. External stimulation also decreased the inhibition by procaine of Ca++ uptake by pool A from 83% to 28%. These results are further evidence that pool A is located in the sarcoplasmic reticulum and that release of pool A to the myofibriles is triggered by excitation-dependent Ca++ influx.
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Hunter et al. (1982) studied Perfused rat heart. Caffeine and procaine was evaluated on Release of cellular calcium pool A. Caffeine (10 mm) rapidly released calcium pool A and decreased its steady state by 60%, while procaine (5 mm) inhibited caffeine-triggered release by 50% in the perfused rat heart.
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