ArticleThe Journal of physiology2001
Acidosis or inorganic phosphate enhances the length dependence of tension in rat skinned cardiac muscle.
Article in The Journal of physiology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
21 citing papers in PubMed, 41 citations in OpenAlex.
- Myosin-actin crossbridge independent sarcomere length induced CaJournal of molecular and cellular cardiology · 2025Article
- CaJournal of molecular and cellular cardiology · 2025Article
- Thermal Activation of Thin Filaments in Striated Muscle.Frontiers in physiology · 2020Review
- The sag response in human muscle contraction.European journal of applied physiology · 2018Article
- Simultaneous imaging of local calcium and single sarcomere length in rat neonatal cardiomyocytes using yellow Cameleon-Nano140.The Journal of general physiology · 2016Article
- Cardiac thin filament regulation and the Frank-Starling mechanism.The journal of physiological sciences : JPS · 2014Review
- Length-dependent effects on cardiac contractile dynamics are different in cardiac muscle containing α- or β-myosin heavy chain.Archives of biochemistry and biophysics · 2013Article
- The constant beat: cardiomyocytes adapt their forces by equal contraction upon environmental stiffening.Biology open · 2013Article
- Enhanced Ca2+ binding of cardiac troponin reduces sarcomere length dependence of contractile activation independently of strong crossbridges.American journal of physiology. Heart and circulatory physiology · 2012Article
- Sarcomere length-dependent Ca2+ activation in skinned rabbit psoas muscle fibers: coordinated regulation of thin filament cooperative activation and passive force.The journal of physiological sciences : JPS · 2011Article
- Regional variation in myofilament length-dependent activation.Pflugers Archiv : European journal of physiology · 2011Review
- Regulatory mechanism of length-dependent activation in skinned porcine ventricular muscle: role of thin filament cooperative activation in the Frank-Starling relation.The Journal of general physiology · 2010Article
- The molecular basis of the steep force-calcium relation in heart muscle.Journal of molecular and cellular cardiology · 2010Review
- Myofilament length dependent activation.Journal of molecular and cellular cardiology · 2010Review
- Protein kinase A-dependent modulation of Ca2+ sensitivity in cardiac and fast skeletal muscles after reconstitution with cardiac troponin.The Journal of general physiology · 2009Article
- Cooperative cross-bridge activation of thin filaments contributes to the Frank-Starling mechanism in cardiac muscle.Biophysical journal · 2009Article
- Titin and troponin: central players in the frank-starling mechanism of the heart.Current cardiology reviews · 2009Article
- Troponin and titin coordinately regulate length-dependent activation in skinned porcine ventricular muscle.The Journal of general physiology · 2008Article
- Disuse-induced preferential loss of the giant protein titin depresses muscle performance via abnormal sarcomeric organization.The Journal of general physiology · 2008Article
- Length-dependent Ca(2+) activation in cardiac muscle: some remaining questions.Journal of muscle research and cell motility · 2005Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1. We investigated the effect of acidosis on the sarcomere length (SL) dependence of tension generation, in comparison with the effect of inorganic phosphate (P(i)), in rat skinned ventricular trabeculae. The shift of the mid-point of the pCa-tension relationship associated with an increase in SL from 1.9 to 2.3 microm (DeltapCa(50)) was studied. 2. Decreasing pH from 7.0 to 6.2 lowered maximal and submaximal Ca(2+)-activated tension and increased DeltapCa(50) in a pH-dependent manner (from 0.21 +/- 0.01 to 0.30 +/- 0.01 pCa units). The addition of P(i) (20 mM) decreased maximal tension and enhanced the SL dependence, both to a similar degree as observed when decreasing pH to 6.2 (DeltapCa(50) increased from 0.20 +/- 0.01 to 0.29 +/- 0.01 pCa units). 3. Further experiments were performed using 6 % (w/v) Dextran T-500 (molecular weight approximately 500 000) to osmotically reduce interfilament lattice spacing (SL, 1.9 microm). Compared with that at pH 7.0, in the absence of P(i) the increase in the Ca(2+) sensitivity of tension induced by osmotic compression was enhanced at pH 6.2 (0.18 +/- 0.01 vs. 0.25 +/- 0.01 pCa units) or in the presence of 20 mM P(i) (0.17 +/- 0.01 vs. 0.24 +/- 0.01 pCa units). 4. H(+), as well as P(i), has been reported to decrease the number of strongly binding cross-bridges, which reduces the co-operative activation of the thin filament and increases the pool of detached cross-bridges available for interaction with actin. It is therefore considered that during acidosis, the degree of increase in the number of force-generating cross-bridges upon reduction of interfilament lattice spacing is enhanced, resulting in greater SL dependence of tension generation. 5. Our results suggest that the Frank-Starling mechanism may be enhanced when tension development is suppressed due to increased H(+) and/or P(i) under conditions of myocardial ischaemia or hypoxia.
Indexed as
Identifiers
What OpenQuestion holds
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.