Perinatal exposure to a high NaCl diet increases the NaCl intake of adult rats

Abstract

To determine the effect of differences in perinatal NaCl exposure on NaCl intake, adult Sprague-Dawley female rats were maintained on diets containing either 0.12, 1.0, or 3% NaCl throughout pregnancy and lactation. The offspring were continued on the these same diets to 30 days postpartum. Thereafter, all offspring were fed the same basal diet containing 1% NaCl. At 90 days of age, the adult offspring were placed in metabolism cages for 7 days and fed 1% NaCl chow for days 1–2, and 0% NaCl chow for days 3–7. On days 6–7, the animals were free to consume both water and 0.3 M NaCl. When dietary NaCl was available, adult rats exposed perinatally to the high NaCl diet excreted significantly more sodium on days 1–2 and 6–7 than did the rats exposed to either the mid or low NaCl diets. There were no differences in sodium excretion during sodium deprivation on days 3–5. The 0.3 M NaCl intake of the high NaCl-exposed rats was also significantly greater than the intake of the mid and low NaCl-exposed rats. In another group of adult rats, exposed perinatally to either a low or high NaCl diet, the spontaneous 24-hr intake of water and 0.3 M NaCl was measured after repeated episodes of acute sodium depletion. Sodium depletion was induced by 48 hr of dietary sodium deprivation combined with a single subcutaneous injection of 5 mg furosemide. Acute sodium depletion was found to augment existing differences in NaCl intake between low and high NaCl-exposed rats. Early NaCl exposure is likely to alter the neuroendocrine mechanisms involved in the control of NaCl intake.