Post-quiescent potentiation (PQP), an enhanced contraction following a long pause that occurs as a result of increased Ca2+ release from intracellular stores, and post-stimulation potentiation (PSP), an enhanced contraction following a rapid series of contractions that is believed to be related to increased Ca2+ influx, were measured in streptozotocin-treated Wistar, spontaneously hypertensive (SHR), and Wistar-Kyoto (WKY) diabetic heart tissues. Decreased PQP values were found in Wistar and SHR diabetic papillary muscles (PM) in comparison with the same strain controls, which suggests a diminished degree of releasable Ca2+ from sarcoplasmic reticulum (SR) in these tissues. Decreased PSP was found in SHR diabetic PM, which may be related primarily to a depressed sarcolemmal (SL) Na(+)-Ca2+ exchange in this tissue. PSP was not decreased in diabetic Wistar or WKY cardiac preparations, indicating that Ca2+ entry via channels must be involved in the PSP mechanism. Ryanodine depressed PQP in Wistar and SHR PM, and SHR left atria in both control and diabetic tissues. It abolished PQP and SHR diabetic tissues but had no effect on WKY control and diabetic tissues. The data suggest that the ryanodine effect differs in the various strains of rat. These differences may be due to differences in the SR sensitivity to ryanodine among the strains. Diabetic SR with impaired Ca2+ uptake may contribute to these phenomena. Ryanodine depressed PSP of Wistar and SHR diabetic PM but had no effects on tissues from controls. The influence of ryanodine on diabetic SL Na(+)-Ca2+ exchange requires further investigation.