Mechanisms of frequency-induced potentiation of contractions in isolated rat atria.

Mechanisms underlying the potentiation of contractions after periods of high frequency stimulation (post-stimulation potentiation; PSP) and periods of rest (rest potentiation; RP) were investigated in isolated rat atria. Transmembrane action potentials were not changed during PSP and RP and were superimposable upon the pre-test action potentials. However, the 45Ca content of atrial strips was significantly increased during PSP, which indicates a net gain in intracellular Ca. 45Ca content was not changed during RP. PSP and RP were increased in magnitude in atria pre-treated with gallopamil (2.5 mumol/l). This effect was due to a greater depression by gallopamil of the pre-test contractions than the potentiated post-test contractions. In contrast, PSP was abolished in atria exposed to 7.5 mmol/l [Ca]o and a transient depression of the post-test contractions was seen. RP was also abolished by high Ca medium, but contractions were not depressed after periods of rest. RP, but not PSP, was unmasked when gallopamil was added to high Ca medium to decrease the size of the basal contractions. Conversely, ryanodine (100 mmol/l) abolished RP but did not affect PSP. With ryanodine present, PSP was greatly increased when the extracellular Ca concentration was increased to 5 mmol/l, whereas RP remained abolished. These results suggest that PSP may reflect an increased transsarcolemmal influx of extracellular Ca, possibly mediated through Na-Ca exchange. In contrast, the mechanism suggested for RP is a transient increase in contractile Ca resulting from an intracellular redistribution of Ca to release sites in the sarcoplasmic reticulum.