The effect of ryanodine on the contraction of isolated frog atrial trabeculae is triggered by caffeine.

Ryanodine is without effect on the contraction of frog atrial muscle when applied alone. However, if agents which bring about Ca2+ release from the sarcoplasmic reticulum (SR), e.g. caffeine, hypertonic fluid or rapid cooling, are applied together with or up to 1 h after exposure to ryanodine, subsequent effects upon contraction are evident. These include a complete inhibition of the contractures evoked by caffeine, rapid cooling or hypertonic solutions applied in Na(+)-deficient media and a shift in the relationship between [Ca2+]o and the strength of the heart beat to a higher [Ca2+]o. The contractures evoked by Na+ withdrawal are unaffected. These results have been interpreted as an action of ryanodine to maintain the open state of the SR Ca(2+)-release channels, thereby inhibiting Ca2+ accumulation by the SR. In this respect the response of the frog heart resembles mammalian heart, but differs in that this action is not triggered by the normal heart beat. These results add support to the notion that, although contraction can be activated in frog atrial muscle by release of Ca2+ from the SR, it is not a major source of Ca2+ during the normal heart beat.