ArticleThe Journal of physiology2003
Normal and pathological excitation-contraction coupling in the heart -- an overview.
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 8 papers.
What it found
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Who cites it
8 citing papers in PubMed.
- Implementation of an epicardial implantable MEMS sensor for continuous and real-time postoperative assessment of left ventricular activity in adult minipigs over a short- and long-term period.APL bioengineering · 2024Article
- Cardiac inotropy, lusitropy, and CaPflugers Archiv : European journal of physiology · 2016Article
- Article
- K201 (JTV-519) alters the spatiotemporal properties of diastolic Ca(2+) release and the associated diastolic contraction during β-adrenergic stimulation in rat ventricular cardiomyocytes.Basic research in cardiology · 2011Article
- Alternans of cardiac calcium cycling in a cluster of ryanodine receptors: a simulation study.American journal of physiology. Heart and circulatory physiology · 2008Article
- Mechanisms of reduced mitochondrial Ca2+ accumulation in failing hamster heart.Pflugers Archiv : European journal of physiology · 2007Article
- Synergistic interactions between Ca2+ entries through L-type Ca2+ channels and Na+-Ca2+ exchanger in normal and failing rat heart.The Journal of physiology · 2005Article
- Regulation of cardiac excitation and contraction by p21 activated kinase-1.Progress in biophysics and molecular biologyReview
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This issue of The Journal of Physiology includes a series of review articles arising from a symposium held at the joint meeting of the UK, German and Scandinavian Physiological Societies. The articles focus on different aspects of the cellular control of contraction. The basic mechanism of cardiac excitation-contraction coupling ('calcium-induced calcium release') is now reasonably well-established. Calcium enters the cell from the extracellular fluid via the voltage-dependent L-type Ca(2+) channel. This results in a 'trigger' increase of [Ca(2+)](i) in the space between the sarcolemma and sarcoplasmic reticulum (SR) and this leads to the opening of the SR Ca(2+) release channel or 'ryanodine receptor' (RyR). As exemplified by the papers from the symposium, much current work is focused on how this mechanism is modified in different circumstances. These include autonomic modulation, but also pathological conditions such as cardiac hypertrophy and failure, a recurrent theme in several of these papers.
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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.