In the heart, intracellular Na+ concentration (Na+i) is a controller of intracellular Ca2+ signaling, and hence of key aspects of cell contractility and rhythm. Na+i will be influenced by variation in Na+ influx. In the present work, we consider one source of Na+ influx, sarcolemmal acid extrusion. Acid extrusion is accomplished by sarcolemmal H+ and HCO3- transporters that import Na+ ions while exporting H+ or importing HCO3-. The capacity of this system to import Na+ is enormous, up to four times the maximum capacity of the Na+-K+ ATPase to extrude Na+ ions from the cell. In this review we consider the role of Na+-H+ exchange (NHE) and Na+-HCO3-co-transport (NBC) in mediating Na+ influx into cardiac myocytes. We consider, in particular, the role of NBC, as so little is known about Na+ influx through this transporter. We show that both proteins mediate significant Na+ influx and that although, in the ventricular myocyte, NBC-mediated Na+ influx is less than through NHE, the proportions may be altered under a variety of conditions, including exposure to catecholamines, membrane depolarization, and interference with activity of the enzyme, carbonic anhydrase.