The DOI matches its Crossref record; 38 of the 38 references it cites were found in a registry or an index.
Ranolazine improves diastolic dysfunction in isolated myocardium from failing human hearts — Role of late sodium current and intracellular ion accumulation
Open accessAbstract
The goal of this study was to test the hypothesis that the novel anti-ischemic drug ranolazine, which is known to inhibit late I(Na), could reduce intracellular [Na(+)](i) and diastolic [Ca(2+)](i) overload and improve diastolic function. Contractile dysfunction in human heart failure (HF) is associated with increased [Na(+)](i) and elevated diastolic [Ca(2+)](i). Increased Na(+) influx through voltage-gated Na(+) channels (late I(Na)) has been suggested to contribute to elevated [Na(+)](i) in HF. In isometrically contracting ventricular muscle strips from end-stage failing human hearts, ranolazine (10 micromol/L) did not exert negative inotropic effects on twitch force amplitude. However, ranolazine significantly reduced frequency-dependent increase in diastolic tension (i.e., diastolic dysfunction) by approximately 30% without significantly affecting sarcoplasmic reticulum (SR) Ca(2+) loading. To investigate the mechanism of action of this beneficial effect of ranolazine on diastolic tension, Anemonia sulcata toxin II (ATX-II, 40 nmol/L) was used to increase intracellular Na(+) loading in ventricular rabbit myocytes. ATX-II caused a significant rise in [Na(+)](i) typically seen in heart failure via increased late I(Na). In parallel, ATX-II significantly increased diastolic [Ca(2+)](i). In the presence of ranolazine the increases in late I(Na), as well as [Na(+)](i) and diastolic [Ca(2+)](i) were significantly blunted at all stimulation rates without significantly decreasing Ca(2+) transient amplitudes or SR Ca(2+) content. In summary, ranolazine reduced the frequency-dependent increase in diastolic tension without having negative inotropic effects on contractility of muscles from end-stage failing human hearts. Moreover, in rabbit myocytes the increases in late I(Na), [Na(+)](i) and [Ca(2+)](i) caused by ATX-II, were significantly blunted by ranolazine. These results suggest that ranolazine may be of therapeutic benefit in conditions of diastolic dysfunction due to elevated [Na(+)](i) and diastolic [Ca(2+)](i).
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Cites
Excitation-Contraction Coupling and Cardiac Contractile Force
Bers, D. M., & Zhu, Y. (2010) · Journal of Cardiovascular Disease Research · doi:10.1016/s0975-3583(10)11011-0 · Cited by 1,603
Excitation-Contraction Coupling and Cardiac Contractile Force
Bers, D. M. (1993) · Developments in Cardiovascular Medicine · doi:10.1007/978-94-017-1512-6 · Cited by 772
Electrophysiological Effects of Ranolazine, a Novel Antianginal Agent With Antiarrhythmic Properties
Antzelevitch, C., Belardinelli, L., Zygmunt, A. C., Burashnikov, A., Di Diego, J. M., Fish, J. M., Cordeiro, J. M., & Thomas, G. (2004) · Circulation · doi:10.1161/01.cir.0000139333.83620.5d · Cited by 675
Self-citationChaitman, B. R., Skettino, S. L., Parker, J. O., Hanley, P., Meluzin, J., Kuch, J., Pepine, C. J., Wang, W., Nelson, J. J., Hebert, D. A., et al. (2004) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2003.11.045 · Cited by 567
Ca2+/calmodulin-dependent protein kinase II regulates cardiac Na+ channels
Wagner, S., Dybkova, N., Rasenack, E. C. L., Jacobshagen, C., Fabritz, L., Kirchhof, P., Maier, S. K. G., Zhang, T., Hasenfuss, G., Brown, J. H., et al. (2006) · Journal of Clinical Investigation · doi:10.1172/jci26620 · Cited by 553
Self-citationValdivia, C. R., Chu, W. W., Pu, J., Foell, J. D., Haworth, R. A., Wolff, M. R., Kamp, T. J., & Makielski, J. C. (2005) · Journal of Molecular and Cellular Cardiology · doi:10.1016/j.yjmcc.2004.12.012 · Cited by 441
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Self-citationBelardinelli, L., Shryock, J. C., & Fraser, H. (2006) · Heart · doi:10.1136/hrt.2005.078790 · Cited by 386
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Senni, M., Paulus, W. J., Gavazzi, A., Fraser, A. G., Diez, J., Solomon, S. D., Smiseth, O. A., Guazzi, M., Lam, C. S. P., Maggioni, A. P., et al. (2014) · European Heart Journal · doi:10.1093/eurheartj/ehu204 · Cited by 355
Sossalla, S., Fluschnik, N., Schotola, H., Ort, K. R., Neef, S., Schulte, T., Wittköpper, K., Renner, A., Schmitto, J. D., Gummert, J., et al. (2010) · Circulation Research · doi:10.1161/circresaha.110.220418 · Cited by 237
Self-citationEmpagliflozin directly improves diastolic function in human heart failure
Pabel, S., Wagner, S., Bollenberg, H., Bengel, P., Kovács, Á., Schach, C., Tirilomis, P., Mustroph, J., Renner, A., Gummert, J., et al. (2018) · European Journal of Heart Failure · doi:10.1002/ejhf.1328 · Cited by 224
Self-citationThe Functional Consequences of Sodium Channel NaV1.8 in Human Left Ventricular Hypertrophy
Ahmad, S., Tirilomis, P., Pabel, S., Dybkova, N., Hartmann, N., Molina, C. E., Tirilomis, T., Kutschka, I., Frey, N., Maier, L. S., et al. (2019) · ESC Heart Failure · doi:10.1002/ehf2.12378 · Cited by 41
Self-citationSchotola, H., Sossalla, S., Rajab, T. K., Toischer, K., Quintel, M., Bauer, M., & Schmitto, J. D. (2011) · Artificial Organs · doi:10.1111/j.1525-1594.2011.01390.x · Cited by 12
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Metadata
- Authors
- Sossalla, S., Wagner, S., Rasenack, E. C. L., Ruff, H., Weber, S. L., Schöndube, F. A., Tirilomis, T., Tenderich, G., Hasenfuss, G., Belardinelli, L., & Maier, L. S.
- Venue
- Journal of Molecular and Cellular Cardiology
- Publisher
- Elsevier BV
- Published
- 2008-07
- Volume
- 45
- Issue
- 1
- Pages
- 32-43
- ISSN
- 0022-2828 (ISSN-L)
- OpenAlex
- W2063954755
- Cited by
- 262
- References
- 38
- FWCI
- 16.06
- Type
- journal article
- Language
- en
- Open access
- green
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- CoChat. (2026). Citation check: Ranolazine improves diastolic dysfunction in isolated myocardium from failing human hearts — Role of late sodium current and intracellular ion accumulation. https://app.cochat.ai/papers/10.1016/j.yjmcc.2008.03.006
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- Sossalla, S., Wagner, S., Rasenack, E. C. L., Ruff, H., Weber, S. L., Schöndube, F. A., Tirilomis, T., Tenderich, G., Hasenfuss, G., Belardinelli, L., & Maier, L. S. (2008). Ranolazine improves diastolic dysfunction in isolated myocardium from failing human hearts — Role of late sodium current and intracellular ion accumulation. Journal of Molecular and Cellular Cardiology. https://doi.org/10.1016/j.yjmcc.2008.03.006
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
