Abstract
Hearts function reasonably well without nerves, but the close match of cardiac output to metabolic demands across a wide range of work loads involves adjustments of the functional properties of the cells by extrinsic regulation involving the autonomic nervous system. Parasympathetic and sympathetic nerves and their neurotransmitters influence not only the frequency of cell beating but also the dynamics of their contraction and relaxation (1,2). The parasympathetic nerves and their neurotransmitter acetylcholine also influence the extent of effects of a given level of sympathetic nervous stimulation (3). As an example of the effects of the autonomic nervous system on the mechanics of heart muscle contraction, Figure 1 shows a schematic of the well-known changes in the twitch dynamics of papillary muscle in response to adrenergic stimulation. Maximum force is increased and the rates of rise and fall of force are increased. These changes reduce overall cycle time and ensure adequate filling of the ventricle in spite of relatively fast heart rates.
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© 1985 Martinus Nijhoff Publishing, Boston
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Solaro, R.J., Garvey, J.L. (1985). Myofilament Protein Phosphorylation and Neural Regulation of Cardiac Contractility. In: Stone, H.L., Weglicki, W.B. (eds) Pathobiology of Cardiovascular Injury. Developments in Cardiovascular Medicine, vol 49. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-2621-2_1
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