ArticleCirculation. Heart failure2009
Multiple defects in intracellular calcium cycling in whole failing rat heart.
Article in Circulation. Heart failure, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 47 citations in OpenAlex.
- Increased SERCA2a sub-cellular heterogeneity in right-ventricular heart failure inhibits excitation-contraction coupling and modulates arrhythmogenic dynamics.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2022Article
- Phosphatidylinositol-4,5-Bisphosphate Binding to Amphiphysin-II Modulates T-Tubule Remodeling: Implications for Heart Failure.Frontiers in physiology · 2021Article
- Oxidative stress creates a unique, CaMKII-mediated substrate for atrial fibrillation in heart failure.JCI insight · 2018Article
- The cardiac ryanodine receptor, but not sarcoplasmic reticulum CaThe Journal of biological chemistry · 2018Article
- T-tubule remodeling and increased heterogeneity of calcium release during the progression to heart failure in intact rat ventricle.Physiological reports · 2017Article
- Triggered intracellular calcium waves in dog and human left atrial myocytes from normal and failing hearts.Cardiovascular research · 2017Article
- Compensatory and decompensatory alterations in cardiomyocyte CaThe Journal of physiology · 2017Article
- Sudden cardiac death in heart failure with preserved ejection fraction: a target for therapy?Heart failure reviews · 2016Review
- 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
- Perspective: a dynamics-based classification of ventricular arrhythmias.Journal of molecular and cellular cardiology · 2015Review
- T-tubule disruption promotes calcium alternans in failing ventricular myocytes: mechanistic insights from computational modeling.Journal of molecular and cellular cardiology · 2015Article
- Reduced mechanical efficiency in left-ventricular trabeculae of the spontaneously hypertensive rat.Physiological reports · 2014Article
- Ultrastructural and cellular basis for the development of abnormal myocardial mechanics during the transition from hypertension to heart failure.American journal of physiology. Heart and circulatory physiology · 2014Article
- Inhibition of the late sodium current slows t-tubule disruption during the progression of hypertensive heart disease in the rat.American journal of physiology. Heart and circulatory physiology · 2013Article
- Electrophysiological and structural determinants of electrotonic modulation of repolarization by the activation sequence.Frontiers in physiology · 2013Article
- Histone deacetylase 1 deficiency impairs differentiation and electrophysiological properties of cardiomyocytes derived from induced pluripotent cells.Stem cells (Dayton, Ohio) · 2012Article
- A network-oriented perspective on cardiac calcium signaling.American journal of physiology. Cell physiology · 2012Review
- Targeted sarcoplasmic reticulum Ca2+ ATPase 2a gene delivery to restore electrical stability in the failing heart.Circulation · 2012Article
- Intracellular Ca2+ waves, afterdepolarizations, and triggered arrhythmias.Cardiovascular research · 2012Article
- Mechanical unloading reverses transverse tubule remodelling and normalizes local Ca(2+)-induced Ca(2+)release in a rodent model of heart failure.European journal of heart failure · 2012Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundA number of defects in excitation-contraction coupling have been identified in failing mammalian hearts. The goal of this study was to measure the defects in intracellular Ca(2+) cycling in left ventricular epicardial myocytes of the whole heart in an animal model of congestive heart failure (CHF). METHODS AND
resultsIntracellular Ca(2+) transients were measured using confocal microscopy in whole rat hearts from age-matched Wistar-Kyoto control rats and spontaneously hypertensive rats at approximately 23 months of age. Basal Ca(2+) transients in myocytes in spontaneously hypertensive rats were smaller in amplitude and longer in duration than Wistar-Kyoto control rats. There was also greater variability in transient characteristics associated with duration between myocytes of CHF than Wistar-Kyoto controls. Approximately 21% of CHF myocytes demonstrated spontaneous Ca(2+) waves compared with very little of this activity in Wistar-Kyoto control rats. A separate population of spontaneously hypertensive rat myocytes showed Ca(2+) waves that were triggered during pacing and were absent at rest (triggered waves). Rapid pacing protocols caused Ca(2+) alternans to develop at slower heart rates in CHF.
conclusionsEpicardial cells demonstrate both serious defects and greater cell-to-cell variability in Ca(2+) cycling in CHF. The defects in Ca(2+) cycling include both spontaneous and triggered waves of Ca(2+) release, which promote triggered activity. The slowing of Ca(2+) repriming in the sarcoplasmic reticulum is probably responsible for the increased vulnerability to Ca(2+) alternans in CHF. Our results suggest that defective Ca(2+) cycling could contribute both to reduced cardiac output in CHF and to the establishment of repolarization gradients, thus creating the substrate for reentrant arrhythmias.
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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.