ArticleThe Journal of physiology1995
Involvement of dihydropyridine receptors in terminating Ca2+ release in rat skeletal myotubes.
Article in The Journal of physiology, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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Who cites it
4 citing papers in PubMed, 16 citations in OpenAlex.
- Skeletal and cardiac ryanodine receptors exhibit different responses to Ca2+ overload and luminal ca2+.Biophysical journal · 2007Article
- Dihydropyridine-induced Ca2+ release from ryanodine-sensitive Ca2+ pools in human skeletal muscle cells.The Journal of physiology · 2000Article
- Effect of nifedipine on depolarization-induced force responses in skinned skeletal muscle fibres of rat and toad.Journal of muscle research and cell motility · 1998Article
- Elementary and global aspects of calcium signalling.The Journal of physiology · 1997Review
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1. Combined patch-clamp and fura-2 measurements were performed in order to investigate the effect of dihydropyridine (DHP) antagonists on termination of sarcoplasmic reticulum (SR) Ca2+ release in cultured rat skeletal myoballs. 2. Ca2+ transients induced by 10 mM caffeine were curtailed by depolarization (e.g. +20 mV for 1 s) and subsequent repolarization (-70 mV). This phenomenon is termed RISC (repolarization-induced stop of caffeine-induced Ca2+ release). 3. At 0.5 to 1 microM, DHP antagonists (nifedipine or (+)PN200-110) strongly inhibited RISC and also slowed the decay of intracellular Ca2+ concentration ([Ca2+]i) following repolarization after depolarization-induced Ca2+ release (-20 or -10 mV for 5 s). 4. The activation time course of the Ca2+ channel associated with the DHP receptor (DHPR) was investigated by measuring DHP-sensitive Ca2+ channel tail currents, while varying the duration of depolarizing pulses. The tail currents increased with pulse duration and peaked around 0.7, 0.9 and 1.1 s for depolarizations to +70, +40 and +20 mV, respectively. These values are compatible with the activation time course of RISC (0.5-1 s to maximally activate RISC at +20 to +60 mV). 5. These results suggest that the DHPR in T-tubular membranes regulates closing of the ryanodine receptor (RyR)-Ca2+ release channel complex through membrane potential change.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.