Introduction: Increased maternal salt intake can lead to hypertension in the offspring. Programmed changes to the renal handling of electrolytes in the adult offspring may underpin this developmental effect. This study tested using in vitro and in vivo models whether moderate maternal salt intake alters fetal kidney development and subsequent structure and function later in life. Methods: Sprague Dawley rats were randomly divided into 2 dietary groups; 1) control diet (CD) fed purified chow and tap water and 2) Salt diet (SD) fed purified chow + 4% NaCl. Animals were fed the diets before during and after (to weaning) gestation. At day 20, a proportion (n=10/diet) was euthanased for biofluid (plasma and amniotic fluid) collection. Remaining litters (n=10 dams/diet) were weaned onto standard chow diet until 9 weeks of age when a proportion (n=5-6 per treatment*sex) were implanted with radiotelemetry probes (TA11PA-C40, Data Sciences Int, USA) for cardiovascular recording or fed chow or salt-diet for 5 days and renal function assessed in metabolic crates. Data are mean [s.e.d] and were analysed by linear mixed-effects models (Genstat v14, VSNi, UK). Results: In vitro murine kidney expansion was marked attenuated (a 1-fold difference) by a 50 mosmole increase in media osmolality (data not shown), but in vivo no effect on fetal kidneys was observed – likely reflecting no difference in fetal plasma osmolality (e.g. fetal plasma: CD, 298 vs. SD, 301 [2] mosmoles/kg water). Salt diet revealed sex-specific programming of blood pressure; SD-males were hypertensive, SD-females were hypotensive relative to CD (mean = 111; treatment × sex effect size = 25 [6] mm Hg). All SD offspring had increased plasma osmolality (SD, 350 vs. CD, 322 [10] mosmoles/kg water) and ECF Na+ (e.g. for SD males, 173 vs. CD males, 147 [6] mmoles/L). Renal salt retention was not different between treatment groups under baseline and salt-loaded conditions but SD offspring had significantly increased plasma corticosterone and proximal colon abundance of SLC9A3 (Fig) – the major glucocorticoid-inducible mechanism for colonic Na+ reabsorption. Conclusions: Maternal high salt intake can have a lifelong effect on offspring blood pressure and Na+ retention, an effect apparently resident in the proximal colon and not the kidneys.