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The permeability and ultrastructure of communicating junctions of cultured neonatal rat ventricular cells are examined under control conditions and during treatments which raise intracellular Ca2+. Lucifer Yellow  (487 mol wt) is used to examine junctional permeability. Under normal ionic conditions dye transfer from an injected muscle cell to neighboring muscle cells occurs rapidly (in less than 6 sec) while transfer to neighboring fibroblasts occurs more slowly. Application of monensin, which results in a partial contracture with superimposed asynchrony, or A23187, which results in a partial contracture, do not inhibit the transfer of dye between the muscle cells. A23187 did result in junctional blockade between muscle cells and fibroblasts. Freeze-fractured gap junctions from control and monensin-treated cells exhibit no distinguishable differences. Center-to-center spacing was not significantly different, 9.0 nm +/- 1.4 SD versus 9.2 nm +/- 1.3 SD, respectively; and particle diameters were virtually unchanged, 8.69 nm +/- 0.9 SD versus 8.61 nm +/- 1.07 SD, respectively. These results suggest that concentrations of intracellular Ca2+ sufficient to support a partial contracture and asynchronous contractile activity do not result in a block of intercellular junctions in cultured myocardial cells. These results are discussed in terms of intracellular Ca2+ -buffering and junctional sensitivity to Ca2+.

Permeability and structural studies of heart cell gap junctions under normal and altered ionic conditions