Lithium, capable of replacing Na+ in various membrane transport processes, was used to investigate Na+ transport pathways across the lamprey erythrocytes membrane. The values of Li+ influxes have ranged from 8 to 24 mmol/l cells/h. Intracellular accumulation of Li+ was associated with loss of cellular Na+, the value of which was less than the value of Li+ influx. Both Li+ influx and Na+ efflux were partially inhibited by amiloride. The amiloride-sensitive Li+ influx was considerably stimulated by hyperosmotic cell shrinkage. The treatment of lamprey erythrocytes with blockers of protein phosphatases (fluoride and cantharidin) also resulted in a considerable increase in Li+ accumulation within the cells. No significant difference was observed between the values of Li+ and Na+ (22Na) influxes measured in red cells incubated simultaneously in isotonic LiCl and NaCl media (9.2 +/- 2.1 and 7.8 +/- 1.3 mmol/l cells/h, respectively). In hypo- and hypertonic media, however, the rate of Na+ influx in lamprey erythrocytes was approximately twice higher as compared to the rate of Li+ influx, what was determined by the difference in the amiloride-sensitive components. In acidified lamprey erythrocytes (intracellular pH 6.0) Li+ and Na+ influxes were considerably increased due to activation of amiloride-sensitive Na+/H+ (Li+/H+) exchange mechanism, although the activity of Na+/H+ exchange was much greater than that of Li+/H+ exchange. The data obtained confirm the hypothesis on the presence of two amiloride-sensitive systems of Na+ transport in the lamprey red blood cells.