ArticleBritish journal of pharmacology2003
SR33805, a Ca2+ antagonist with length-dependent Ca2+ -sensitizing properties in cardiac myocytes.
Article in British journal of pharmacology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Regioselective C2-Sulfonylation of Indoles and Pyrroles via SOOrganic letters · 2026Article
- High-Throughput Screens of Repurposing Hub and DOS Chemical Libraries Reveal Compounds with Novel and Potent Inhibitory Activity Against the Essential Non-Neuronal Acetylcholinesterase ofInternational journal of molecular sciences · 2025Article
- [3 + 2]-Annulation of pyridinium ylides with 1-chloro-2-nitrostyrenes unveils a tubulin polymerization inhibitor.Organic & biomolecular chemistry · 2021Article
- The fast and efficient KI/HRSC advances · 2018Article
- Exploring cardiac biophysical properties.Global cardiology science & practice · 2015Article
- Inotropes and inodilators for acute heart failure: sarcomere active drugs in focus.Journal of cardiovascular pharmacology · 2014Review
- Beneficial effects of SR33805 in failing myocardium.Cardiovascular research · 2011Article
- Regional variation in myofilament length-dependent activation.Pflugers Archiv : European journal of physiology · 2011Review
- The cAMP binding protein Epac regulates cardiac myofilament function.Proceedings of the National Academy of Sciences of the United States of America · 2009Article
- Blebbistatin: use as inhibitor of muscle contraction.Pflugers Archiv : European journal of physiology · 2008Article
Corrections and comments
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Authors and funding
4 authors.
Funding
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Abstract
1. This study examined the effects of SR33805, a fantofarone derivative with reported strong Ca(2+) -antagonistic properties, on the contractile properties of intact and skinned rat ventricular myocytes. 2. On intact cells loaded with the Ca(2+)-fluorescent indicator Indo-1, the application of low concentrations of SR33805 enhanced the amplitude of unloaded cell shortening and decreased the duration of cell shortening. Amplitude of the Ca(2+) transient was also decreased. 3. These effects were accompanied with a shortening of the action potential and a dose-dependent blockade of L-type calcium current (IC(50)=2.4 x 10(-8) M). 4. On skinned cardiac cells, the application of a low SR33805 concentration (10(-8) M) induced a significant increase in maximal Ca(2+)-activated force at the two-tested sarcomere lengths (SLs), 1.9 and 2.3 microm. 5. The application of a larger dose of SR33805 (10(-6)-10(-5) M) induced a significant leftward shift of the tension-pCa relation that accounts for Ca(2+)-sensitization of the myofilaments, particularly at 2.3 microm SL. 6. In conclusion, despite its strong Ca(2+)-antagonistic properties SR33805 increases cardiac cell contractile activity as a consequence of its Ca(2+)-sensitizing effects. These effects are attributable to both an increase in the maximal Ca(2+)-activated force and a length-dependent Ca(2+)-sensitization.
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