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...

Full description

Bibliographic Details
Main Authors: Cros, Caroline, Sallé, Laurent, Warren, Daniel E., Shiels, Holly A., Brette, Fabien
Format: Online
Language:English
Published: American Physiological Society 2014
Online Access:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4269670/
id pubmed-4269670
recordtype oai_dc
spelling 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