The myocardial cell surface, its histochemistry, and the effect of sialic acid and calcium removal on its stucture and cellular ionic exchange.

Abstract

The surfaces of neonatal rat cells in culture, neonatal rat hearts and adult rabbit hearts have qualitatively similar responses to La, ruthenium red and colloidal Fe stains. All demonstrate a surface coat and external lamina with abundant negatively charged sites. Cells with intact surface structure do not permit entry of La3+ intracellularly. The surface of all the myocardial cells studied contained abundant sialic acid distributed in 2 distinct layers, 1 in the surface coat next to the lipid bilayer, the other in the external lamina at the interstitial interface. The removal of sialic acid from the cellular surface increases Ca2+ exchangeability 5- to 6-fold. Its removal permits La3+ to enter the cell and displace more than 80% of cellular Ca2+. Despite these marked alterations in Ca2+ and La3+ permeability, sialic acid removal has no effect on K+ permeability. This indicates that the integrity of surface coat is critical in the regulation of Ca2+ (and La3+) exchange, but that K+ permeability is controlled at the bilayer region. Exposure of the cells to [Ca2+]0 = 5 .mu.M produces a change in the surface. A peeling of the external lamina from the surface coat occurs with separation of the 2 sialic acid layers and the formation of a fluid-filled bleb between them. Ca2+ removal apparently ruptures Ca- carbohydrate couplings (e.g., fucose-Ca-fucose bridges) which may anchor the external lamina to the surface coat. The effect of Ca2+ removal on ionic permeability is not specific. The cell demonstrates increased permeability to La3+ and K+. This indicates that Ca2+ depletion affects the surface structure and the bilayer region.