ArticleThe Journal of physiology2002
Effects of phosphocreatine on SR Ca(2+) regulation in isolated saponin-permeabilized rat cardiac myocytes.
Article in The Journal of physiology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed, 14 citations in OpenAlex.
- Protective Effects of Dinitrosyl Iron Complexes under Oxidative Stress in the Heart.Oxidative medicine and cellular longevity · 2017Article
- The Golgi apparatus is a functionally distinct Ca2+ store regulated by the PKA and Epac branches of the β1-adrenergic signaling pathway.Science signaling · 2015Article
- Local energetic regulation of sarcoplasmic and myosin ATPase is differently impaired in rats with heart failure.The Journal of physiology · 2008Article
- Cytosolic energy reserves determine the effect of glycolytic sugar phosphates on sarcoplasmic reticulum Ca2+ release in cat ventricular myocytes.The Journal of physiology · 2006Article
- Altered energy transfer from mitochondria to sarcoplasmic reticulum after cytoarchitectural perturbations in mice hearts.The Journal of physiology · 2006Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The effects of phosphocreatine (PCr) on sarcoplasmic reticulum (SR) Ca(2+) regulation were investigated in saponin-permeabilized rat ventricular myocytes. Cells were perfused continuously with weakly Ca(2+)-buffered solutions approximating to the intracellular milieu. Ca(2+) release from the SR was detected using Fura-2 or Fluo-3. Withdrawal of PCr reduced the frequency of spontaneous Ca(2+) release by 12.8 +/- 3.4 % (n = 9) and the amplitude of the spontaneous Ca(2+) transient by 17.4 +/- 3.1 % (n = 9). Stepwise reductions in [PCr] progressively increased the time for the spontaneous Ca(2+) transient to rise from 25 to 100 % of the maximum value (TP75) and to fall by 75 % of the peak level (DT75). Following complete PCr withdrawal, the TP75 and the DT75 were 147.1 +/- 13.2 and 174.8 +/- 23.2 % of the control values, respectively. Experiments involving confocal microscopy showed that PCr withdrawal decreased the propagation velocity of spontaneous Ca(2+) waves. PCr withdrawal also reduced the frequency and amplitude, but increased the duration of spontaneous Ca(2+) sparks. Rapid application of 20 mM caffeine was used to assess the SR Ca(2+) content at the point of spontaneous Ca(2+) release. In the absence of PCr, the amplitude of the caffeine-induced Ca(2+) transient was 18.4 +/- 2.7 % (n = 9) lower than in the presence of 10 mM PCr. This suggests that PCr withdrawal reduces the maximum SR Ca(2+) content that can be sustained before spontaneous Ca(2+) release occurs. These results suggest that local ADP buffering by PCr is essential for normal Ca(2+) regulation by the SR. Prolongation of the descending phase of the spontaneous Ca(2+) transient is consistent with a reduction in the efficiency of the SR Ca(2+) pump due to ADP accumulation. The fact that spontaneous Ca(2+) release occurs at a lower SR Ca(2+) content in the absence of PCr suggests that the Ca(2+) release mechanism may also be affected. These effects may be of relevance in circumstances where PCr depletion and Ca(2+) overload occur, such as myocardial ischaemia or anoxia.
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