Diffusion restriction in murine cardiac myocytes depends on mouse strain and is enhanced by deletion of VDAC1 porin channels (35°C). “CD” indicates myocytes from CD1/J6/129svJ mice. (A) Representative records of Na/K pump current decline using patch pipettes without MgATP for CD WT and CD/VDAC1-deficient myocytes. (B) Composite results. Decline of Na/K pump current is more than twofold faster in CD WT myocytes than in BL6 WT myocytes. Pump current decline is twofold slower in CD myocytes lacking VDAC1 than in CD WT myocytes. Results were similar using either 80 or 20 mM cytoplasmic Na. (C) Micrographs of CD WT and VDAC1-deficient myocytes after 10 min of patch clamp with 10 µM carboxyfluorescein. The longitudinal fluorescence gradient is still pronounced in the myocyte lacking VDAC1 after 10 min. (D) Similar to results for Na/K pump currents, the time constant with which carboxyfluorescein equilibrates in BL6 WT myocytes is more than twofold greater than in CD WT myocytes, and the time constant is more than twofold greater in CD myocytes lacking VDAC1 than in WT CD myocytes. **P < 0.01.