An isometric muscle preparation was used to study the inhibitory effect of ryanodine on contractile function in isolated ventricular trabeculae of the Pacific mackerel (Scomber japonicus). Ryanodine (an inhibitor of sarcoplasmic reticulum (SR) function) caused a 20% reduction in peak tension at 20 o C, but not 15 o C, over the range of frequencies (0.2-3.0 Hz) tested. This indicates that in the absence of a functional SR, the mackerel ventricle can maintain most of its contractile strength utilizing other modes of Ca 2 + delivery to the myofilaments. Ca 2 + flux through the sarcolemmal (SL) L-type Ca 2 + -channels is most likely the predominant pathway for Ca 2 + activation of the myofilaments, although reverse mode Na + /Ca 2 + exchange could potentially contribute to a significant extent. High levels of adrenergic stimulation overwhelmed the negative inotropy caused by ryanodine, returning tension to pre-ryanodine levels, further suggesting that the mackerel ventricle can maintain contractile function without Ca 2 + contribution from the SR. These results are discussed within the context of what is known about SR Ca 2 + utilization in rainbow trout and tuna hearts.