The DOI matches its Crossref record; 32 of the 32 references it cites were found in a registry or an index.
Rate Dependence of [Na + ] i and Contractility in Nonfailing and Failing Human Myocardium
Open accessAbstract
Background — In the failing human heart, altered Ca 2+ homeostasis causes contractile dysfunction. Because Ca 2+ and Na + homeostasis are intimately linked through the Na + /Ca 2+ exchanger, we compared the regulation of [Na + ] i in nonfailing (NF) and failing human myocardium. Methods and Results — [Na + ] i was measured in SBFI-loaded muscle strips. At slow pacing rates (0.25 Hz, 37°C), isometric force was similar in NF (n=6) and failing (n=12) myocardium (6.4±1.2 versus 7.2±1.9 mN/mm 2 ), but [Na + ] i and diastolic force were greater in failing (22.1±2.6 mmol/L and 15.6±3.2 mN/mm 2 ) than in NF (15.9±3.1 mmol/L and 3.50±0.55 mN/mm 2 ; P <0.05) myocardium. In NF hearts, increasing stimulation rates resulted in a parallel increase in force and [Na + ] i without changes in diastolic tension. At 2.0 Hz, force increased to 136±17% of the basal value ( P <0.05), and [Na + ] i to 20.5±4.2 mmol/L ( P <0.05). In contrast, in failing myocardium, force declined to 45±3%, whereas [Na + ] i increased to 27.4±3.2 mmol/L (both P <0.05), in association with significant elevations in diastolic tension. [Na + ] i was higher in failing than in NF myocardium at every stimulation rate. [Na + ] i predicted in myocytes from Na + pipette -contraction relations was 8.0 mmol/L in NF (n=9) and 12.1 mmol/L in failing (n=57; P <0.05) myocardium at 0.25 Hz. Reverse-mode Na + /Ca 2+ exchange induced significant Ca 2+ influx in failing but not NF myocytes, compatible with higher [Na + ] i in failing myocytes. Conclusions — Na + i homeostasis is altered in failing human myocardium. At slow heart rates, the higher [Na + ] i in failing myocardium appears to enhance Ca 2+ influx through Na + /Ca 2+ exchange and maintain sarcoplasmic reticulum Ca 2+ load and force development. At faster rates, failing myocytes with high [Na + ] i cannot further increase sarcoplasmic reticulum Ca 2+ load and are prone to diastolic Ca 2+ overload.
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Cites
Cardiac excitation–contraction coupling
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Excitation-Contraction Coupling and Cardiac Contractile Force
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Self-citationJBeuckelmann, D., MNäbauer, & EErdmann (1992) · Circulation · Cited by 662
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Self-citationAltered myocardial force-frequency relation in human heart failure.
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Self-citationAlterations of Sarcoplasmic Reticulum Proteins in Failing Human Dilated Cardiomyopathy
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Cited by
Paulus, W. J., Tschöpe, C., Sanderson, J. E., Rusconi, C., Flachskampf, F. A., Rademakers, F. E., Marino, P., Smiseth, O. A., De Keulenaer, G., Leite-Moreira, A. F., et al. (2007) · European Heart Journal · doi:10.1093/eurheartj/ehm037 · Cited by 2,679
Self-citationO'Hara, T., Virág, L., Varró, A., & Rudy, Y. (2011) · PLoS Computational Biology · doi:10.1371/journal.pcbi.1002061 · Cited by 1,196
Mitochondrial function as a therapeutic target in heart failure
Brown, D. A., Perry, J. B., Allen, M. E., Sabbah, H. N., Stauffer, B. L., Shaikh, S. R., Cleland, J. G. F., Colucci, W. S., Butler, J., Voors, A. A., et al. (2017) · Nature Reviews Cardiology · doi:10.1038/nrcardio.2016.203 · Cited by 803
Self-citationCa2+/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-citationMechanisms of Altered Ca 2+ Handling in Heart Failure
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Metadata
- Authors
- Pieske, B., Maier, L. S., Piacentino, V., Weisser, J., Hasenfuss, G., & Houser, S.
- Venue
- Circulation
- Published
- 2002-07-23
- Volume
- 106
- Issue
- 4
- Pages
- 447-453
- ISSN
- 0009-7322 (ISSN-L)
- 1524-4539
- OpenAlex
- W2159730220
- Cited by
- 305
- References
- 32
- FWCI
- 9.76
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Pieske, B., Maier, L. S., Piacentino, V., Weisser, J., Hasenfuss, G., & Houser, S. (2002). Rate Dependence of [Na + ] i and Contractility in Nonfailing and Failing Human Myocardium. Circulation. https://doi.org/10.1161/01.cir.0000023042.50192.f4
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