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First published online June 13, 2008
Journal of Experimental Biology 211, 2005-2013 (2008)
Published by The Company of Biologists 2008
doi: 10.1242/jeb.003145

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Commentary

The Frank–Starling mechanism in vertebrate cardiac myocytes

Holly A. Shiels^1,* and Ed White²

¹ Faculty of Life Sciences, Core Technology Facility, 46 Grafton Street, University of Manchester, Manchester M13 9NT, UK
² Institute of Membrane and Systems Biology, University of Leeds, Leeds LS2 9JT, UK

^* Author for correspondence (e-mail: holly.shiels{at}manchester.ac.uk)

Accepted 10 April 2008

The Frank–Starling law of the heart applies to all classes of vertebrates. It describes how stretch of cardiac muscle, up to an optimum length, increases contractility thereby linking cardiac ejection to cardiac filling. The cellular mechanisms underlying the Frank–Starling response include an increase in myofilament sensitivity for Ca²⁺, decreased myofilament lattice spacing and increased thin filament cooperativity. Stretching of mammalian, amphibian and fish cardiac myocytes reveal that the functional peak of the sarcomere length (SL)–tension relationship occurs at longer SL in the non-mammalian classes. These findings correlate with in vivo cardiac function as non-mammalian vertebrates, such as fish, vary stroke volume to a relatively larger extent than mammals. Thus, it seems the length-dependent properties of individual myocytes are modified to accommodate differences in organ function, and the high extensibility of certain hearts is matched by the extensibility of their myocytes. Reasons for the differences between classes are still to be elucidated, however, the structure of mammalian ventricular myocytes, with larger widths and higher levels of passive stiffness than those from other vertebrate classes may be implicated.

Key words: sarcomere length–tension relationship, mammals, birds, reptiles, amphibians, fish

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