Abstract
Conductance of myocardial gap junctions is controlled by divalent cations, such as Ca2+ and Mg2+in addition to the trans-junctional potential. Although the steady-state dose-dependency is available, kinetics of the chemical gating is not determined. Thus, it is difficult to estimate the gap junctional conductance during the Ca2+ transient accompanying the cardiac contraction. We applied the two-electrodes voltage clamp technique to one of the paired ventricular myocytes (cell 1) isolated from hearts, and measured clamp currents evoked by ±5 mV test pulses from a holding potential of 0 mV. After replacing the external solution to a Cs+-rich intracellular solution containing a given concentration of divalent cation, the membrane of the paired cell (cell 2) was instantaneously ruptured by applying a pulse of nitrogen laser near the gap junction. We first examined effects of Mg2+ because Mg2+ does not induce contraction or the Ca2+ release from SR, and is not influenced by the intracellular Ca2+ buffer. Immediately after rupturing the cell 2 membrane, the input conductance was enlarged to a peak of (220∼730) nS from a steady level of (8∼70) nS before the rupture. In the presence of divalent cations, the conductance then decreased over the following several seconds in a [Mg2+]-dependent manner. The conductance decay was best fit by a sum of two exponential functions with time constants of 3 and 106 sec at 10 mM [Mg2+]. [Jpn J Physiol 55 Suppl:S132 (2005)]
