Frog ventricle: Participation of SR in excitation-contraction coupling

Activation of the first beat (B₁) following a 60-s pause is diminished in isometrically contracting frog ventricular strips, in contrast to the augmentation documented for sarcoplasmic reticulum (SR)-dependent mammalian myocardium. However, treatment of frog ventricular strips with ouabain, an indirect inhibitor of the sarcolemmal Na⁺-Ca²⁺ exchanger, selectively enhanced postpause beats suggesting that in the absence of ouabain significant extrusion of cellular Ca²⁺ occurred during the pause. Because resting tension did not increase during the pause in ouabain-treated strips, the nonextruded Ca²⁺ must have been sequestered into a compartment such as SR. Steady-state beats were not affected by ouabain; its actions appeared to be separate from its known positive inotropism. Caffeine, a direct SR stimulus, initially enhanced B₁ and subsequently decreased activation of all beats, which was consistent with initial augmentation of SR Ca²⁺ release and subsequent depletion of SR Ca²⁺ stores. Ouabain both potentiated the stimulatory effects and blocked the inhibitory effects of caffeine, suggesting that ouabain increased Ca²⁺ stores in the same intracellular Ca²⁺ pool as that acted on by caffeine, the SR. Ryanodine, an inhibitor of SR in mammalian myocardium, did not affect activation of frog myocardium. SR may be an important site for activator Ca²⁺ cycling in frog myocardium under control conditions as well as after long diastolic intervals in the presence of ouabain.