Cardiomyocyte contraction depends on rapid changes in intracellular Ca(2+). In 
mammals, Ca(2+) influx as L-type Ca(2+) current (ICa) triggers the release of 
Ca(2+) from sarcoplasmic reticulum (SR) and Ca(2+)-induced Ca(2+) release (CICR) 
is critical for excitation-contraction coupling. In fish, the relative 
contribution of external and internal Ca(2+) is unclear. Here, we characterized 
the role of ICa to trigger SR Ca(2+) release in rainbow trout ventricular 
myocytes using ICa regulation by Ca(2+) as an index of CICR. ICa was recorded 
with a slow (EGTA) or fast (BAPTA) Ca(2+) 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 Ca(2+), 
while with isoproterenol, inactivation was Ca(2+)-dependent (∼65%) and highly 
reliant on SR Ca(2+) (∼46%). Thus, SR Ca(2+) is not released in basal 
conditions, and ICa is the main trigger of contraction, whereas during a stress 
response, SR Ca(2+) is an important source of cytosolic Ca(2+). This was not 
attributed to differences in SR Ca(2+) load because caffeine-induced transients 
were not different in both conditions. Therefore, Ca(2+) 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.