Toggle Main Menu Toggle Search

Open Access padlockePrints

Pressure-calcium relationships in perfused mouse hearts

Lookup NU author(s): Dr Guy MacGowanORCiD, Charlotte Evans

Downloads

Full text for this publication is not currently held within this repository. Alternative links are provided below where available.


Abstract

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.


Publication metadata

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


Altmetrics

Altmetrics provided by Altmetric


Funding

Funder referenceFunder name
HL 03826NHLBI NIH HHS
HL 68083NHLBI NIH HHS
T32 HL 76124NHLBI NIH HHS

Share