The calcium stored in the sarcoplasmic reticulum acts as a safety mechanism in rainbow trout heart
Cardiomyocyte contraction depends on rapid changes in intracellular Ca2+. In mammals, Ca2+ influx as L-type Ca2+ current (ICa) triggers the release of Ca2+ from sarcoplasmic reticulum (SR) and Ca2+-induced Ca2+ release (CICR) is critical for excitation-contraction coupling. In fish, the relative con...
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American Physiological Society
2014
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Online Access: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4269670/ |
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pubmed-42696702014-12-24 The calcium stored in the sarcoplasmic reticulum acts as a safety mechanism in rainbow trout heart Cros, Caroline Sallé, Laurent Warren, Daniel E. Shiels, Holly A. Brette, Fabien Cardiovascular and Renal Integration Cardiomyocyte contraction depends on rapid changes in intracellular Ca2+. In mammals, Ca2+ influx as L-type Ca2+ current (ICa) triggers the release of Ca2+ from sarcoplasmic reticulum (SR) and Ca2+-induced Ca2+ release (CICR) is critical for excitation-contraction coupling. In fish, the relative contribution of external and internal Ca2+ is unclear. Here, we characterized the role of ICa to trigger SR Ca2+ release in rainbow trout ventricular myocytes using ICa regulation by Ca2+ as an index of CICR. ICa was recorded with a slow (EGTA) or fast (BAPTA) Ca2+ chelator in control and isoproterenol conditions. In the absence of β-adrenergic stimulation, the rate of ICa inactivation was not significantly different in EGTA and BAPTA (27.1 ± 1.8 vs. 30.3 ± 2.4 ms), whereas with isoproterenol (1 μM), inactivation was significantly faster with EGTA (11.6 ± 1.7 vs. 27.3 ± 1.6 ms). When barium was the charge carrier, inactivation was significantly slower in both conditions (61.9 ± 6.1 vs. 68.0 ± 8.7 ms, control, isoproterenol). Quantification revealed that without isoproterenol, only 39% of ICa inactivation was due to Ca2+, while with isoproterenol, inactivation was Ca2+-dependent (∼65%) and highly reliant on SR Ca2+ (∼46%). Thus, SR Ca2+ is not released in basal conditions, and ICa is the main trigger of contraction, whereas during a stress response, SR Ca2+ is an important source of cytosolic Ca2+. This was not attributed to differences in SR Ca2+ load because caffeine-induced transients were not different in both conditions. Therefore, Ca2+ stored in SR of trout cardiomyocytes may act as a safety mechanism, allowing greater contraction when higher contractility is required, such as stress or exercise. American Physiological Society 2014-11-05 2014-12-15 /pmc/articles/PMC4269670/ /pubmed/25377479 http://dx.doi.org/10.1152/ajpregu.00127.2014 Text en Copyright © 2014 the American Physiological Society Licensed under Creative Commons Attribution CC-BY 3.0 (http://creativecommons.org/licenses/by/3.0/deed.en_US) : © the American Physiological Society. |
repository_type |
Open Access Journal |
institution_category |
Foreign Institution |
institution |
US National Center for Biotechnology Information |
building |
NCBI PubMed |
collection |
Online Access |
language |
English |
format |
Online |
author |
Cros, Caroline Sallé, Laurent Warren, Daniel E. Shiels, Holly A. Brette, Fabien |
spellingShingle |
Cros, Caroline Sallé, Laurent Warren, Daniel E. Shiels, Holly A. Brette, Fabien The calcium stored in the sarcoplasmic reticulum acts as a safety mechanism in rainbow trout heart |
author_facet |
Cros, Caroline Sallé, Laurent Warren, Daniel E. Shiels, Holly A. Brette, Fabien |
author_sort |
Cros, Caroline |
title |
The calcium stored in the sarcoplasmic reticulum acts as a safety mechanism in rainbow trout heart |
title_short |
The calcium stored in the sarcoplasmic reticulum acts as a safety mechanism in rainbow trout heart |
title_full |
The calcium stored in the sarcoplasmic reticulum acts as a safety mechanism in rainbow trout heart |
title_fullStr |
The calcium stored in the sarcoplasmic reticulum acts as a safety mechanism in rainbow trout heart |
title_full_unstemmed |
The calcium stored in the sarcoplasmic reticulum acts as a safety mechanism in rainbow trout heart |
title_sort |
calcium stored in the sarcoplasmic reticulum acts as a safety mechanism in rainbow trout heart |
description |
Cardiomyocyte contraction depends on rapid changes in intracellular Ca2+. In mammals, Ca2+ influx as L-type Ca2+ current (ICa) triggers the release of Ca2+ from sarcoplasmic reticulum (SR) and Ca2+-induced Ca2+ release (CICR) is critical for excitation-contraction coupling. In fish, the relative contribution of external and internal Ca2+ is unclear. Here, we characterized the role of ICa to trigger SR Ca2+ release in rainbow trout ventricular myocytes using ICa regulation by Ca2+ as an index of CICR. ICa was recorded with a slow (EGTA) or fast (BAPTA) Ca2+ chelator in control and isoproterenol conditions. In the absence of β-adrenergic stimulation, the rate of ICa inactivation was not significantly different in EGTA and BAPTA (27.1 ± 1.8 vs. 30.3 ± 2.4 ms), whereas with isoproterenol (1 μM), inactivation was significantly faster with EGTA (11.6 ± 1.7 vs. 27.3 ± 1.6 ms). When barium was the charge carrier, inactivation was significantly slower in both conditions (61.9 ± 6.1 vs. 68.0 ± 8.7 ms, control, isoproterenol). Quantification revealed that without isoproterenol, only 39% of ICa inactivation was due to Ca2+, while with isoproterenol, inactivation was Ca2+-dependent (∼65%) and highly reliant on SR Ca2+ (∼46%). Thus, SR Ca2+ is not released in basal conditions, and ICa is the main trigger of contraction, whereas during a stress response, SR Ca2+ is an important source of cytosolic Ca2+. This was not attributed to differences in SR Ca2+ load because caffeine-induced transients were not different in both conditions. Therefore, Ca2+ stored in SR of trout cardiomyocytes may act as a safety mechanism, allowing greater contraction when higher contractility is required, such as stress or exercise. |
publisher |
American Physiological Society |
publishDate |
2014 |
url |
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4269670/ |
_version_ |
1613168533281177600 |