Programmed aortic dysfunction and reduced Na + ,K + ‐ATPase activity present in first generation offspring of lard‐fed rats does not persist to the second generation

We have previously reported that male and female offspring of Sprague–Dawley rats fed a diet rich (approximately 50% of caloric intake from fat) in animal fat (lard) during pregnancy and suckling (OHF) demonstrate cardiovascular dysfunction, including blunted endothelium‐dependent vasodilatation in the aorta as well as reduced renal Na + ,K + ‐ATPase activity. Cardiovascular dysfunction has been reported in other models of developmental programming and some researchers describe transmission from F 1 to F 2 generations. Here we report a study of vascular function, as assessed in isolated rings of aorta mounted in an organ bath, and renal Na + ,K + ‐ATPase activity in 6‐month‐old male and female F 2 offspring of lard‐fed and control‐fed (OC) dams ( n = 13 per diet group). An increase in brain (OC 0.61 ± 0.01% versus OHF 0.66 ± 0.02% of bodyweight) and kidney weights (OC 0.32 ± 0.01% versus OHF 0.37 ± 0.01% of bodyweight) was observed in female F 2 offspring of lard‐fed dams compared with F 2 controls ( P < 0.03). Constrictor responses to phenylephrine in the aorta were not different from F 2 controls (repeated measures ANOVA, P = 0.85). Also, endothelium‐dependent dilator function, as assessed by responses to acetylcholine (repeated measures ANOVA, P = 0.96) and passive distensibility in the absence of extracellular calcium (repeated measures ANOVA, P = 0.68), was similar. Additionally, renal Na + ,K + ‐ATPase activity was not statistically different from that observed in control animals (ANOVA, P = 0.89). Although a maternal diet rich in animal fat has deleterious effects on parameters of cardiovascular risk in F 1 animals, it does not appear that disorders previously reported in the F 1 generation are transmitted to the F 2 generation.