ArticleThe Journal of physiology2003
Reduced contraction strength with increased intracellular [Ca2+] in left ventricular trabeculae from failing rat hearts.
Article in The Journal of physiology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 44 citations in OpenAlex.
- Measurement of Intracellular CaMethods in molecular biology (Clifton, N.J.) · 2025Article
- Impaired calcium handling mechanisms in atrial trabeculae of diabetic patients.Physiological reports · 2023Article
- Quantitative high-throughput assay to measure MC4R-induced intracellular calcium.Journal of molecular endocrinology · 2021Article
- Stretch modulation of cardiac contractility: importance of myocyte calcium during the slow force response.Biophysical reviews · 2020Review
- Disruption of Transverse-Tubules Eliminates the Slow Force Response to Stretch in Isolated Rat Trabeculae.Frontiers in physiology · 2020Article
- Zinc transporter 10 (ZnT10)-dependent extrusion of cellular MnThe Journal of biological chemistry · 2019Article
- Calcium mishandling impairs contraction in right ventricular hypertrophy prior to overt heart failure.Pflugers Archiv : European journal of physiology · 2018Article
- Mitochondria and cardiovascular diseases-from pathophysiology to treatment.Annals of translational medicine · 2018Review
- Highly variable contractile performance correlates with myocyte content in trabeculae from failing human hearts.Scientific reports · 2018Article
- Does reduced myocardial efficiency in systemic hypertensive-hypertrophy correlate with increased left-ventricular wall thickness?Hypertension research : official journal of the Japanese Society of Hypertension · 2015Article
- Sex differences in stretch-dependent effects on tension and Ca(2+) transient of rat trabeculae in monocrotaline pulmonary hypertension.The journal of physiological sciences : JPS · 2015Article
- Mitochondrial injury and dysfunction in hypertension-induced cardiac damage.European heart journal · 2014Review
- Reduced mechanical efficiency in left-ventricular trabeculae of the spontaneously hypertensive rat.Physiological reports · 2014Article
- Protection of the heart by treatment with a divalent-copper-selective chelator reveals a novel mechanism underlying cardiomyopathy in diabetic rats.Cardiovascular diabetology · 2013Article
- Myocardial twitch duration and the dependence of oxygen consumption on pressure-volume area: experiments and modelling.The Journal of physiology · 2012Article
- Excitation-contraction coupling in ventricular myocytes is enhanced by paracrine signaling from mesenchymal stem cells.Journal of molecular and cellular cardiology · 2012Article
- Stimulatory effects of calcium on respiration and NAD(P)H synthesis in intact rat heart mitochondria utilizing physiological substrates cannot explain respiratory control in vivo.The Journal of biological chemistry · 2011Article
- Ablation of phospholamban and sarcolipin results in cardiac hypertrophy and decreased cardiac contractility.Cardiovascular research · 2011Article
- Early development of intracellular calcium cycling defects in intact hearts of spontaneously hypertensive rats.American journal of physiology. Heart and circulatory physiology · 2010Article
- Non-steady-state calcium handling in failing hearts from the spontaneously hypertensive rat.Pflugers Archiv : European journal of physiology · 2010Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Intracellular calcium ([Ca2+](i)) and isometric force were measured in left ventricular (LV) trabeculae from spontaneously hypertensive rats (SHR) with failing hearts and normotensive Wistar-Kyoto (WKY) controls. At a physiological stimulation frequency (5 Hz), and at 37 degrees C, the peak stress of SHR trabeculae was significantly (P < or = 0.05) reduced compared to WKY (8 +/- 1 mN mm(-2) (n = 8) vs. 21 +/- 5 mN mm(-2) (n = 8), respectively). No differences between strains in either the time-to-peak stress, or the time from peak to 50 % relaxation were detected. Measurements using fura-2 showed that in the SHR both the peak of the Ca2+ transient and the resting [Ca2+](i) were increased compared to WKY (peak: 0.69 +/- 0.08 vs. 0.51 +/- 0.08 microM(P < or = 0.1) and resting: 0.19 +/- 0.02 vs. 0.09 +/- 0.02 microM(P < or = 0.05), SHR vs. WKY, respectively). The decay of the Ca2+ transient was prolonged in SHR, with time constants of: 0.063 +/- 0.002 vs. 0.052 +/- 0.003 s (SHR vs. WKY, respectively). Similar results were obtained at 1 Hz stimulation, and for [Ca2+ ](o) between 0.5 and 5 mM. The decay of the caffeine-evoked Ca2+ transient was slower in SHR (9.8 +/- 0.7 s (n = 8) vs. 7.7 +/- 0.2 s (n = 8) in WKY), but this difference was removed by use of the SL Ca2+ -ATPase inhibitor carboxyeosin. Histological examination of transverse sections showed that the fractional content of perimysial collagen was increased in SHR compared to WKY (18.0 +/- 4.6 % (n = 10) vs. 2.9 +/- 0.9 % (n = 11) SHR vs. WKY, respectively). Our results show that differences in the amplitude and the time course of the Ca2+ transient between SHR and WKY do not explain the reduced contractile performance of SHR myocardium per se. Rather, we suggest that, in this animal model of heart failure, contractile function is compromised by increased collagen, and its three-dimensional organisation, and not by reduced availability of intracellular Ca2+.
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