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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
journal contributionposted on 2007-05-01, 00:00 authored by James ArmitageJames Armitage, A Ishibashi, A A Balachandran, R I Jensen, L Poston, P D Taylor
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 F1 to F2 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 F2 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 F2 offspring of lard-fed dams compared with F2 controls (P < 0.03). Constrictor responses to phenylephrine in the aorta were not different from F2 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 F1 animals, it does not appear that disorders previously reported in the F1 generation are transmitted to the F2 generation.