The impact of chronic low-sodium intake during early development on body sodium homeostasis is not sufficiently known. To explore this effect, we have investigated the influence of chronic sodium deficit during the rapid growth period of rats (first phase, age 3-7 wk) and the short-term effect of sodium repletion (second phase, age 8-9 wk) on parameters such as growth rate, urinary aldosterone excretion, 22Na volume of distribution (space), and various renal functions. Three groups were studied: group I (control) and groups II and III. During the first phase the respective sodium intake values for these groups were 8.9, 3.1, and 1.5 meq.kg body wt-1.day-1. During the second phase, all groups had sodium intake of 8.7-8.8 meq.kg body wt-1.day-1. At the end of the first phase, group II showed weight gain and 22Na space values similar to those of group I. Group III demonstrated severe growth retardation and reduced 22Na space. During the second phase, both groups II and III demonstrated expansion of the 22Na space and persistently elevated urinary 'acid-labile' aldosterone excretions. Despite the 2 wk of sodium repletion, group III failed to catch up with the body weight of groups I and II. It is concluded that chronic sodium deficit during early development greatly influences sodium and aldosterone homeostasis once a transition is made to a higher sodium intake.
|Original language||English (US)|
|Journal||American Journal of Physiology - Endocrinology and Metabolism|
|State||Published - 1982|
All Science Journal Classification (ASJC) codes
- Physiology (medical)
- Endocrinology, Diabetes and Metabolism