The isolated rabbit sinus node was partly divided into two parts by a cut in the middle portion. Microelectrode recording near the bridge connecting the two parts revealed an interference between action potentials from the two parts. Comparison of microelectrode recordings from the two parts taken near the bridge suggested that an induced peculiar rhythm change in one part was probably induced by the electrotonic effects of the action potentials of the other part. To prove this, a subthreshold depolarizing square-wave pulse was applied extracellularly to the isolated uncut sinus node. When the pulse was applied in the early portion of slow diastolic depolarization, diastole was prolonged, and when it was applied in the later portion, diastole was shortened. These findings can explain the observed peculiar thythm and suggest that in the mammalian sinus node, pacemaker cells accelerate or decelerate mutually by the electrotonic effects of their action potentials, depending on the phase of application of the effects. In particular, for some time the faster pacemaker cells could be influenced by dragging effects from the neighboring slower pacemaker cells and the slower pacemaker cells by pulling effects from the neighboring faster pacemaker cells.
We studied conduction properties and histological findings at branching sites of the pectinate muscle (PM) from the crista terminalis (CT) in the dog right atrium. Propagation was faster in the longitudinal direction along CT than along PM. When the rate of stimulation was increased, conduction blocks to PM occurred at a longer cycle length than those to CT in 10 of 19 cases without differences in the refractory period. There were two block sites, one at the lateral edge within CT and the other at the branching site of PM from CT. The former was dominant with normal solution and the latter with high K+ solution. Histological studies showed no apparent differences between the two groups. CT consisted of a number of unit bundles in a longitudinal direction. The unit bundles continuing from the edge of CT proceeded into PM. Their orientation in PM, however, became irregular and tangled. Between the branches of PM, conduction block occurred unpredictably without regard to direction. These observations indicated the importance of the arrangement and orientation of the unit bundles in the appearance of the preferential conduction and block.
Effects of extracellular magnesium (Mg2+) on action potential duration (APD) and underlying membrane currents in guinea pig ventricular myocytes were studied by using the whole cell patch-clamp method. Increasing external Mg2+ concentration [Mg2+]o) from 0.5 to 3 mM produced a prolongation of APD at 90% repolarization (APD90), whereas 5 and 10 mM Mg2+ shortened it. [Mg2+]o, at 3 mM or higher, suppressed the delayed outward K+ current and the inward rectifier K+ current. Increases in [Mg2+]o depressed the peak amplitude and delayed the decay time course of the Ca2+ current (ICa), the latter effect is probably due to the decrease in Ca(2+)-induced inactivation. Thus 3 mM Mg2+ suppressed the peak ICa but increased the late ICa amplitude at the end of a 200-ms depolarization pulse, whereas 10 mM Mg2+ suppressed both components. Application of 10 mM Mg2+ shifted the voltage-dependent activation and inactivation by approximately 10 mV to more positive voltage due to screening the membrane surface charges. Application of manganese (1-5 mM) also caused dual effects on APD90, similar to those of Mg2+, and suppressed the peak ICa with slowed decay. These results suggest that the dual effects of Mg2+ on APD in guinea pig ventricular myocytes can be, at least in part, explained by its action on ICa with slowed decay time course in addition to suppressive effects on K+ currents.
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