Na+ influx mechanisms in submandibular salivary cells of newborn rats.

Uptake of this isotopic tracer was essentially the same as in cells derived from salivary glands of adult animals, both in the absence and in the presence of 1 microM acetylcholine, 10 microM monensin or 10 microM A23187. Tracer accumulation in resting cells was inhibited in the immature cells by 1 mM amiloride but the inhibition was significantly smaller than in fully mature cells (16 and 33%, respectively). Bumetanide inhibited tracer uptake by 28% in mature cells not exposed to agonist, but had essentially no effect in those of newborn rats. The tracer content of adult cells exposed to acetylcholine in Ca(2+)-free incubation solutions was significantly reduced when compared to that of cells exposed to agonist in solutions containing 1.0 mM CaCl2. A similar but significantly smaller reduction in tracer content was observed in cells of newborn animals incubated in the Ca(2+)-free medium. The inhibition of 22Na uptake observed in the presence of amiloride was the same in both types of cells in the presence or absence of external Ca2+. The findings suggest that Na entry into immature salivary cells of newborn rats is quantitatively similar to that in mature cells, but that the contribution of the loop diuretic-sensitive co-transporter and of the amiloride-sensitive Na/H exchange to Na+ entry is less in the immature cells. Na entry in the immature cells is likely to occur, therefore, primarily by other mechanisms such as Ca(2+)-regulated channels.