Abstract

The rabbit A-V node was dissected into pieces (0.2 x 0.2 x 0.2 mm) smaller than its space constant of 692 +/- 96 micrometers (n = 5). These small specimens showed spontaneous action potentials whose configurations were similar to those of large specimens before dissection. The membrane time constant was 21.5 +/- 1.5 ms (n = 5). Voltage clamp experiments were performed on the above specimens using the two-microelectrode technique. On depolarization from the holding potential of -40 mV to various potential levels a transient inward current and delayed outward current were recorded. On repolarization an outward current tail was observed. The transient inward current was blocked by application of D 600 (2 x 10(-7) g/ml) but was insensitive to TTX (1 x 10(-7) g/ml). The inward current was decreased by superfusion with Na- or Ca-free Tyrode solution. Thus, this current was classified as the slow inward current (is). When the K concentration in the Tyrode solution was varied, the reversal potential of the outward current tail changed as expected for a K electrode, indicating that the outward current was carried by K ions. On hyperpolarization slow activation of inward current was recorded. The reversal potential of this current was between -20 and -30 mV, which was analogous to hyperpolarization activated current, ih, in the S-A node. A contribution of sodium current (iNa) to the action potential was obviously demonstrated from an inhibitory effect of TTX on the upstroke of the anodal break excitation. The ionic selectivity of each current system is compared with analogous current systems in other cardiac tissues and a possible mechanism for the slow conduction in the A-V node is discussed.

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