Suppressive role of Na⁢-Ca2⁢ exchange in myocardial tension generation was examined in the negative frequency-force relationship (FFR) of electric field stimulated left atria (LA) from postnatal developing rat heart and in the whole-cell clamped adult rat ventricular myocytes with high concentration of intracellular Ca2⁢ buffer (14 mM EGTA). LA twitch amplitudes, which were suppressed by cyclopiazonic acid in a postnatal age-dependent manner, elicited frequency-dependent and postnatal age-dependent enhancements after Na⁢-reduced, Ca2⁢-depleted (26 Na-0 Ca) buffer application. These enhancements were blocked by caffeine pretreatment with postnatal age-dependent intensities. In the isolated rat ventricular myocytes, stimulation with the voltage protocol roughly mimicked action potential generated a large inward current which was partially blocked by nifedipine or Na⁢ current inhibition. 0 Ca application suppressed the inward current by 39⁑4% while the current was further suppressed after 0 Na-0 Ca application by 53⁑3%. Caffeine increased this inward current by 44⁑3% in spite of 14 mM EGTA. Finally, the Na⁢ current-dependent fraction of the inward current was increased in a stimulation frequency-dependent manner. From these results, it is concluded that the Ca2⁢ exit-mode (forward-mode) Na⁢-Ca2⁢ exchange suppresses the LA tension by extruding Ca2⁢ out of the cell right after its release from sarcoplasmic reticulum (SR) in a frequency-dependent manner during contraction, resulting in the negative frequency-force relationship in the rat LA.