Normal and pathological excitation-contraction coupling in the heart -- an overview.
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.
Eisner
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DA
Cardiac Physiology Unit, Stopford Building, University of Manchester, Manchester M13 9PT, UK.
Isenberg
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G
Sipido
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D000200:Action Potentials; D000818:Animals; D006321:Heart / Q000502:physiology* / Q000503:physiopathology*; D006331:Heart Diseases / Q000503:physiopathology*; D006801:Humans; D009200:Myocardial Contraction / Q000502:physiology*; D009569:Nitric Oxide / Q000378:metabolism; D019001:Nitric Oxide Synthase / Q000378:metabolism; D052250:Nitric Oxide Synthase Type III
D009569:Nitric Oxide; C496314:NOS3 protein, human; D019001:Nitric Oxide Synthase; D052250:Nitric Oxide Synthase Type III