The ectoderm of the one-day chick embryo generates dorsoventrally oriented short-circuit current (Isc) entirely dependent on extracellular sodium. At the dorsal cell membrane, the Isc was modified reversibly and in a concentration-dependent manner by: amiloride (60% decrease at 1 mM, with 2 apparent IC50S: 0.13 and 48 microM), phlorizin (0.1 mM) or removal of glucose (30% decrease, additive to that of amiloride), SITS (1 mM, 13% decrease). Acidification of alkalinization of the dorsal (but not ventral) superfusate produced, respectively, decrease or increase of Isc with a pH50 of 7.64. Ba2+ (0.1-1 mM) from either side of the ectoderm decreased the Isc by 30%. Anthracene-9-carboxylic acid, furosemide and inducers of cAMP had no effect on electrophysiological properties of the blastoderm. The chick ectoderm is therefore a highly polarized epithelium containing, at the dorsal membrane, the high and low affinity amiloride-sensitive Na+ channels, Na(+)-glucose cotransporter, K+ channels and pH sensitivity, and, at the ventral membrane, the Na+, K(+)-ATPase and K+ channels. The Na+ transport reacts to pH, but lacks the cAMP regulatory system, well known in many epithelia. The active Na+ transport drives glucose and fluid into the intraembryonic space, across and around the blastoderm which, in the absence of blood circulation, could secure renewal of extracellular fluid and disposal of wastes and thus maintain the cell homeostasis.