It has been suggested that the sodium-calcium exchanger, Ncx1, may have a greater physiological role in embryonic and neonatal hearts than in adult heart. However, in chick heart sarcolemmal vesicles, sodium-dependent calcium transport is reported to be small, and, moreover, to be 3-12 times smaller in hearts at embryonic day (ED) 4-5 day than at ED18, the opposite of what would be expected of a transporter that is more important in early development. To better assess the role of Ncx1 in calcium regulation in the chick embryonic heart we measured the activity of Ncx1 in chick embryonic hearts as Ca²⁺_o -activated exchanger current (I_NCX) under controlled ionic conditions. With [Ca²⁺]_i = 47 nM, I_NCX density increased from 1.34 ± .28 pA/pF at ED2 to 3.22 ± .55 pA/pF at ED11 (P = 0.006), but with[Ca²⁺]_i = 481 nM the increase was small and statistically insignificant, from 4.54 ± 0.77 to 5.88 ± .73 (P = 0.20, E_m = 0 mV, [Ca²⁺]_o = 2 mM). Plots of I_NCX density against [Ca²⁺]_i were well fitted by the Michaelis-Menton equation and extrapolated to identical maximal currents for ED2 and ED11 cells ([Ca²⁺]_o = 1, 2 or 4 mM). Thus, the increase in I_NCX at low [Ca²⁺]_i appeared to reflect a developmental change in allosteric regulation of the exchanger by Ca²⁺_i rather than an increase in the membrane density of Ncx1. Supporting this conclusion, RT-PCR demonstrated little change in the amount of mRNA encoding Ncx1 expression from ED2 through ED18.