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Lookup NU author(s): Dr Guy MacGowanORCiD, Charlotte Evans
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We explored the relationship between left ventricular (LV) pressure and intracellular free calcium concentration ([Ca]i) in the isolated perfused mouse heart. [Ca]i (rhod-2) and LV pressure were recorded simultaneously. In response to increases in LV volume (Frank-Starling, FS, protocol), there were increases in developed pressure (up to 250%), with no changes in pressure morphology (rise or relaxation time) or [Ca]i (magnitude and morphology) for up to 10 min. During transient increases in the stimulus interval at a fixed LV volume (mechanical restitution, MR, protocol), developed pressure increased significantly (31.3 ± 1.2%), with relatively small changes in peak systolic [Ca]i (7.4 ± 1.4%). The relaxation of [Ca]i, however, was prolonged (30.0 ± 5.5%), resulting in prolonged pressure relaxation (21.2 ± 1.9%) and increased area under the calcium transient that paralleled the increase in developed pressure (1:1 ratio). A model-based analysis showed that changes in LV pressure during the MR protocol could be completely explained by altered [Ca] i; it was not necessary to invoke any changes in model parameters (i.e., dynamic processes that link calcium to pressure). For the FS data, the model predicted only a change in the gain parameter; however, this change alone cannot reproduce well-established length-dependent changes in the steadystate force-pCa relationship. In summary, the mouse myocardium appears to be unique in that significant changes in peak developed pressure can occur with little or no change in the peak [Ca]i. Additionally, unlike other mammalian species, load-dependent prolongation of pressure relaxation is absent in the mouse heart, and pressure relaxation is primarily governed by intracellular free calcium relaxation. Copyright © 2006 the American Physiological Society.
Author(s): MacGowan GA, Kirk JA, Evans C, Shroff SG
Publication type: Article
Publication status: Published
Journal: American Journal of Physiology: Heart and Circulatory Physiology
Year: 2006
Volume: 290
Issue: 6
Pages: H2614-H2624
ISSN (print): 0363-6135
ISSN (electronic): 1522-1539
Publisher: American Physiological Society
URL: http://dx.doi.org/10.1152/ajpheart.00979.2005
DOI: 10.1152/ajpheart.00979.2005
PubMed id: 16415077
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