ArticleBritish journal of pharmacology1999
Differential effects of bepridil on functional properties of troponin C in slow and fast skeletal muscles.
Article in British journal of pharmacology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed, 14 citations in OpenAlex.
- Early Deconditioning of Human Skeletal Muscles and the Effects of a Thigh Cuff Countermeasure.International journal of molecular sciences · 2021Article
- 3-Chlorodiphenylamine activates cardiac troponin by a mechanism distinct from bepridil or TFP.The Journal of general physiology · 2019Article
- Novel myosin-based therapies for congenital cardiac and skeletal myopathies.Journal of medical genetics · 2016Review
- Probing the mechanism of cardiovascular drugs using a covalent levosimendan analog.Journal of molecular and cellular cardiology · 2016Article
- Targeting the sarcomere to correct muscle function.Nature reviews. Drug discovery · 2015Review
- The role of the Ca(2+) regulatory sites of skeletal troponin C in modulating muscle fibre reactivity to the Ca(2+) sensitizer bepridil.British journal of pharmacology · 2000Article
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1. Bepridil (BPD) is a pharmacological compound able to bind to the Ca2+ sensor protein troponin C (TnC), which triggers skeletal muscle contraction upon Ca2+-binding. BPD can thereby modulate the Ca2+-affinity of this protein. 2. The Ca2+-sensitizing action of bepridil was investigated on slow and fast isoforms of TnC from skinned slow and fast skeletal muscle fibres, activated by either Ca2+ or Sr2+ ions. 3. Bepridil did not modify the Ca2+ maximal tension of slow and fast fibres, suggesting that binding of the drug to TnC did not induce a change in the number of cross-bridges involved in maximal tension. 4. Sr2+ ions induced lower maximal tension than Ca2+ ions. However, in fast fibres, these lower Sr2+ maximal tensions could be reinforced by bepridil, suggesting an effect of bepridil on the function of site I of fast TnC. 5. Under submaximal tension, bepridil induced an increase in Ca2+ affinity of TnC in both slow and fast fibres. However, slow fibres were more drug reactive than fast fibres, and the increase in tension appeared to be modulated by the Ca2+ concentration. 6. Thus, bepridil exerted a differential effect on slow and fast fibres. Moreover, the results suggest that bepridil was more effective when activation conditions were unfavourable.
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Registered trials
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.