{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T20:24:51Z","timestamp":1791318291999,"version":"4.3.1"},"reference-count":60,"publisher":"American Physiological Society","issue":"12","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Regulatory, Integrative and Comparative Physiology"],"published-print":{"date-parts":[[2014,12,15]]},"abstract":"<jats:p>Cardiomyocyte contraction depends on rapid changes in intracellular Ca<jats:sup>2+<\/jats:sup>. In mammals, Ca<jats:sup>2+<\/jats:sup>influx as L-type Ca<jats:sup>2+<\/jats:sup>current ( I<jats:sub>Ca<\/jats:sub>) triggers the release of Ca<jats:sup>2+<\/jats:sup>from sarcoplasmic reticulum (SR) and Ca<jats:sup>2+<\/jats:sup>-induced Ca<jats:sup>2+<\/jats:sup>release (CICR) is critical for excitation-contraction coupling. In fish, the relative contribution of external and internal Ca<jats:sup>2+<\/jats:sup>is unclear. Here, we characterized the role of I<jats:sub>Ca<\/jats:sub>to trigger SR Ca<jats:sup>2+<\/jats:sup>release in rainbow trout ventricular myocytes using I<jats:sub>Ca<\/jats:sub>regulation by Ca<jats:sup>2+<\/jats:sup>as an index of CICR. I<jats:sub>Ca<\/jats:sub>was recorded with a slow (EGTA) or fast (BAPTA) Ca<jats:sup>2+<\/jats:sup>chelator in control and isoproterenol conditions. In the absence of \u03b2-adrenergic stimulation, the rate of I<jats:sub>Ca<\/jats:sub>inactivation was not significantly different in EGTA and BAPTA (27.1 \u00b1 1.8 vs. 30.3 \u00b1 2.4 ms), whereas with isoproterenol (1 \u03bcM), inactivation was significantly faster with EGTA (11.6 \u00b1 1.7 vs. 27.3 \u00b1 1.6 ms). When barium was the charge carrier, inactivation was significantly slower in both conditions (61.9 \u00b1 6.1 vs. 68.0 \u00b1 8.7 ms, control, isoproterenol). Quantification revealed that without isoproterenol, only 39% of I<jats:sub>Ca<\/jats:sub>inactivation was due to Ca<jats:sup>2+<\/jats:sup>, while with isoproterenol, inactivation was Ca<jats:sup>2+<\/jats:sup>-dependent (\u223c65%) and highly reliant on SR Ca<jats:sup>2+<\/jats:sup>(\u223c46%). Thus, SR Ca<jats:sup>2+<\/jats:sup>is not released in basal conditions, and I<jats:sub>Ca<\/jats:sub>is the main trigger of contraction, whereas during a stress response, SR Ca<jats:sup>2+<\/jats:sup>is an important source of cytosolic Ca<jats:sup>2+<\/jats:sup>. This was not attributed to differences in SR Ca<jats:sup>2+<\/jats:sup>load because caffeine-induced transients were not different in both conditions. Therefore, Ca<jats:sup>2+<\/jats:sup>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.<\/jats:p>","DOI":"10.1152\/ajpregu.00127.2014","type":"journal-article","created":{"date-parts":[[2014,11,7]],"date-time":"2014-11-07T08:22:10Z","timestamp":1415348530000},"page":"R1493-R1501","source":"Crossref","is-referenced-by-count":22,"title":["The calcium stored in the sarcoplasmic reticulum acts as a safety mechanism in rainbow trout heart"],"prefix":"10.1152","volume":"307","author":[{"given":"Caroline","family":"Cros","sequence":"first","affiliation":[{"name":"Faculty of Life Sciences, The University of Manchester, Core Technology Facility, Manchester, United Kingdom; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Laurent","family":"Sall\u00e9","sequence":"additional","affiliation":[{"name":"EA 4650, Universit\u00e9 de Caen, Caen Cedex, 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