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

Area of Science:

• Cardiovascular Physiology
• Cell Biology
• Biophysics

Background:

• Communicating junctions (gap junctions) are crucial for coordinated heart cell function.
• Intracellular calcium (Ca2+) plays a vital role in cardiac contractility and cell signaling.
• Understanding how Ca2+ affects junctional permeability is key to comprehending cardiac electrophysiology.

Purpose of the Study:

• To investigate the impact of elevated intracellular Ca2+ on the permeability and structure of gap junctions in cultured neonatal rat ventricular cells.
• To determine if increased Ca2+ levels, sufficient to induce contracture, lead to junctional blockade between cardiac cells.

Main Methods:

• Utilized Lucifer Yellow dye to assess intercellular permeability between neonatal rat ventricular cells and fibroblasts.
• Applied chemical treatments (monensin, A23187) to increase intracellular Ca2+ levels and induce cellular responses.
• Examined the ultrastructure of gap junctions using freeze-fracture electron microscopy on control and treated cells.

Main Results:

• Dye transfer between cardiac muscle cells was rapid and unaffected by treatments that raised intracellular Ca2+.
• A23187 treatment caused junctional blockade specifically between muscle cells and fibroblasts, but not between muscle cells themselves.
• Freeze-fracture analysis revealed no significant differences in gap junction spacing or particle size between control and treated cells.

Conclusions:

• Elevated intracellular Ca2+ concentrations, even those causing partial contracture and asynchronous activity, do not inhibit gap junction communication between cultured myocardial cells.
• The findings suggest that myocardial gap junctions possess a degree of resilience to changes in intracellular Ca2+.
• Further research is needed to fully elucidate the mechanisms of intracellular Ca2+-buffering and junctional sensitivity in cardiac tissue.