Fig. 2. Development and recovery of inactivated human heart (hH1) channels from block by bupivacaine enantiomers. (A ) A conditioning pulse to −70 mV of variable duration was applied. A 100-ms interval at the holding potential of −160 mV was then inserted before delivery of the test pulse to +30 mV to evoke the Na⁺currents. Control currents (open circles) and currents in the presence of 10 μm R  (+)- (filled squares) and S  (−)-bupivacaine (filled diamonds) were normalized to the current obtained without a preceding conditioning pulse to −70 mV. Solid lines represent fits of the data to a single exponential function. (B ) Recovery from block of inactivated hH1 Na⁺channels by bupivacaine enantiomers. Cells were conditioned with a 10-s depolarizing pulse to −70 mV from a holding potential of −160 mV. Recovery was determined by applying a test pulse to +30 mV at various times after the conditioning pulse. The data were normalized to the amplitude of the test pulse obtained after 50-s recovery time. The data were best fitted by the sum of two exponentials. The control data (open circles) for experiments with R  (+)- and S  (−)-bupivacaine were combined. hH1 wild-type currents in the absence of drugs (open squares) recoverd with fast (Τ1) and slow time constants (Τ2) of 2.8 ± 0.2 ms and 0.06 ± 0.01 s, respectively. Inactivated hH1 wild-type channels recovered from block by 10 μm R  (+)-bupivacaine (filled squares; n = 5) with Τ1 = 7.3 ± 1.1 ms and Τ2 = 2.1 ± 0.1 s and from block by S  (−)-bupivacaine (filled diamonds; n = 5) with Τ1 = 7.2 ± 1.1 ms and Τ2 = 1.3 ± 0.1 s.