Several studies support the hypothesis that chronic diseases in adulthood might be triggered by events that occur during fetal development. This study examined the consequences of perinatal salt intake on blood pressure (BP) and carbohydrate and lipid metabolism in adult offspring of dams on high-salt [HSD; 8% (HSD2) or 4% (HSD1)], normal-salt (NSD; 1.3%), or low-salt (LSD; 0.15% NaCl) diet during pregnancy and lactation. At 12 wk of age, female Wistar rats were matched with adult male rats that were fed NSD. Weekly tail-cuff BP measurements were performed before, during, and after pregnancy. After weaning, the offspring received only NSD and were housed in metabolic cages for 24-h urine collection for sodium and potassium and nitrate and nitrite excretion measurements. At 12 wk of age, intra-arterial mean BP was measured, a euglycemic-hyperinsulinemic clamp was performed, and plasma lipids and nitrate and nitrite concentrations were determined. Tail-cuff BP was higher during pregnancy in HSD2 and HSD1 than in NSD and LSD dams. Mean BP (mm Hg) was also higher in the offspring of HSD2 (110 Ϯ 5) and HSD1 (107 Ϯ 5) compared with NSD (100 Ϯ 2) and LSD (92 Ϯ 2). Lower glucose uptake and higher plasma cholesterol and triacylglycerols were observed in male offspring from LSD dams (glucose uptake: HSD2 17 Ϯ 4, HSD1 15 Ϯ 3, NSD 11 Ϯ 3, LSD 4 Ϯ 1 mg · kg Ϫ1 · min Ϫ1 ; cholesterol: HSD2 62 Ϯ 6, HSD1 82 Ϯ 11, NSD 68 Ϯ 10, LSD 98 Ϯ 17 mg/dL; triacylglycerols: HSD2 47 Ϯ 15, HSD1 49 Ϯ 12, NSD 56 Ϯ 19, LSD 83 Ϯ 11 mg/dL). In conclusion, maternal salt intake during pregnancy and lactation has long-term influences on arterial pressure, insulin sensitivity, and plasma lipids of the adult offspring. (Pediatr Res 56: 842-848, 2004) Abbreviations BP, blood pressure HSD, high-salt diet HR, heart rate LSD, low-salt diet MBP, mean blood pressure NSD, normal-salt diet NOx, nitrate plus nitrite RAS, renin-angiotensin system tcBP, tail-cuff blood pressure Almost two decades ago, Barker and Osmond (1) proposed that ischemic heart disease could be triggered by events that occur during fetal life and early childhood (1). They showed an association between poor living standard during the perinatal period and ischemic heart disease in adulthood. This lifestyle possibly goes along with intrauterine growth retardation. Despite criticisms about the validity of their observations (2), the association between low birth weight and adult diseases is now further supported by several studies with similar findings (3-6). Moreover, the understanding of the mechanisms of this association represents a challenge for investigators in this area.Intrauterine growth is controlled by a complex interplay of maternal and fetal factors, including circulatory, endocrine, and metabolic systems (7). An increasing number of studies have shown that small modifications in fetal growth may have profound consequences in later life (8 -10).
