Did not differ in between offspring from WT and Leprdb/+ dams, no matter offspring diet program (Fig 4A?D). Endothelial-independent I-CBP112 vasodilation was also tested, and no important differences were observed for SNPinduced vasodilation amongst any from the groups (Fig 4E?H). Endothelial-dependent vasodilation responses of mesenteric arteries to ACh (Fig 5A?D) and insulin (Fig 5E?H) have been also assessed. When offspring were fed a SD, these born to WT and Leprdb/+ dams exhibited no variations in ACh-induced vasodilation (Fig 5A). Nevertheless, offspring of WT dams had greater (P<0.05) vasodilatory responses to ACh when fed a HFDFig 3. Effect of maternal environment on mesenteric artery responses to vasoactive agonists. The elastic properties of mesenteric arteries were affected by a (maternal environment) x (offspring diet) interaction. We further examined the structural properties of mesenteric arteries to determine if the observed differences in vasodilation were associated with differences in vascular remodeling. No differences in vascular structural characteristics were observed in juvenile offspring (Fig 6). In adult mice, mesenteric vascular remodeling in response to HFD differed between WT male offspring from Leprdb/+ and WT-control dams. In offspring fed a SD, the passive luminal diameter of arteries was significantly greater (P<0.05) in offspring of Leprdb/+ dams than in offspring from WT dams (Fig 7A). HFD feeding significantly increased passive luminal diameters and CSAs in offspring from WT dams (Fig 7C and 7G), but not in offspring from Leprdb/+ dams (Fig 7D and 7H). As a result, on HFD, the CSA was significantly reduced (P<0.05) in offspring of Leprdb/+ dams versus that from WT dams (Fig 7F). No differences were observed in the arterial wall-to-lumen ratios among any of the groups (data not shown). Arterial stiffness was affected by maternal environment, and diet had an effect depending on maternal environment. Offspring of Leprdb/+ dams had significantly reduced (P<0.05) vascular wall strain values (Fig 8A and 8B) and higher moduli of elasticity (Fig 8E and 8F), indicative of arterial stiffness compared to offspring of WT dams. There were no differences in vascular wall stress (Fig 8C and 8D) or elastic moduli (Fig 8G and 8H) between diets. To investigate arterial stiffness at low pressures, we analyzed arterial compliance (Fig 8I?L) and the low-modulus of elasticity (Fig 8I?L, insets). The low-modulus of elasticity in mesenteric arteries from offspring of Leprdb/+ dams was increased (P<0.05) compared to offspring of WT dams, when offspring were fed a HFD (Fig 8J, inset). This effect of HFD was correlated with a tendency for an increased vascular compliance at low pressures (Fig 8J); however, the difference in compliance did not reach statistical significance. No other significant effects of maternal environment or diet on arterial compliance or the low-modulus of elasticity were observed. Thus, maternal hyperleptinemia increased arterial stiffness at high pressures, independent of offspring diet, whereas at low pressures, there was a (maternal environment) x (offspring diet) interaction, such that offspring of WT, but not Leprdb/+ dams, PubMed ID:http://www.ncbi.nlm.nih.gov/pubmed/21179575 had reduced arterial stiffness (enhanced compliance) in response to HFD.The structural composition of mesenteric resistance arteries was impacted by a (maternal atmosphere) x (offspring diet regime) interactionThe cytoskeletal and extracellular matrix composition of blood vessels straight impacts vascular struct.