Abstract
Rats drinking a combination of taurine and hypertonic saline solution rapidly develop hypernatremia, but rats drinking either solution alone do not. The mechanism by which taurine disrupts the ability to deal with a salt load is not clear. Rats housed in metabolism cages were studied. Food intake, fluid intake, plasma sodium concentration, urine output, sodium balance, visible water balance, and urine osmolality were determined over a period of 8 days. Rats drinking 0.1 M taurine plus 1.8% NaCl developed a mean plasma sodium concentration of 160±18 mM by Day 6, compared with 137±1.6 mM in water drinking controls. Ingestion of 1.8% saline alone produced only a mild, transient rise in plasma sodium(<150 mM), which returned to control levels by Day 8. Ingestion of neither 0.1 M taurine alone nor 0.1 M β-alanine, a taurine transport antagonist, produced any evidence of hypernatremia throughout the experiment. When β-alanine was added to the taurine + saline regimen, mean plasma sodium reached only 149±16 mM (Day 6). Inspection of the ratio of cumulative sodium balance to cumulative water balance revealed a rapid increase until Day 2, followed by a virtual plateau thereafter in the taurine + saline group. Rats drinking saline alone showed an equally rapid rise in the ratio, but to a lower plateau level, suggesting that taurine exerts a much more pronounced disturbance of sodium balance than of water balance. The addition of β-alanine to the regimens of taurine + saline or saline alone produced ratios of cumulative sodium to cumulative water balance significantly lower than that of either regimen without β-alanine. These findings suggest that taurine induces hypernatremia by interfering with normal homeo-static control mechanisms and that β-alanine counteracts that action of taurine.
