The permeability of rat heart myocytes to Na increases when extracellular Ca (Ca0) is decreased. This increased permeability is reflected in elevated Na/K ratios in nonenergized myocytes and in increased ouabain-sensitive lactate production in anaerobic myocytes supplemented with glucose. Myocytes treated with ethylene glycol bis(beta-aminoethyl ether)N,N'-tetraacetic acid (1 mM) maintain low Na/K ratios, but expend considerable glycolytic ATP in ouabain-sensitive cation cycling. The data suggest that Ca0 bound to the sarcolemma can restrict transmembrane movement of Na via pathways that are not yet defined. The lack of significant net accumulation of Ca argues against the explanation that Ca0 maintains low internal Na levels as a result of Na-Ca exchange. Both the increased uptake of Na and increased utilization of ATP in the absence of Ca0 may be relevant to the phenomenon of "Ca-paradox" in situ.