Objectives : Our previous study showed that estrogen played an important role in limiting cardiovascular dysfunction induced by maternal protein restriction. Therefore, we hypothesized that estrogen replacement therapy (ERT) would improve the cardiovascular dysfunction of ovariectomized offspring following maternal protein restriction.
Methods : Wistar rats were fed a diet containing either 18% (control group;C) or 9% casein (protein restriction group : R) throughout pregnancy only. On day 50, the offspring in the C and R groups were divided into 3 groups each, and the indicated surgery was performed in each group (sham group (CO, RO), ovariectomized group (CX, RX), ovariectomized and ERT group (CE, RE). On day 50, 75,100,125,150,175, blood pressure was measured in all groups. On day 175, the offspring were killed and the mesenteric arteries dissected. Endothelial function in the mesenteric artery was investigated with a wire myograph in all groups. Vascular contraction to cumulative dose-responses to phenylephrine (PE) and the thromboxane A2 mimetic, U46619 were carried out under isometric conditions. Endothelium-dependent relaxation was assessed by acetylcholine (ACh), and bradykinin (BK) -induced relaxation in the PE pre-contracted arteries. Endothelium-independent relaxation was determined by sodium nitroprusside (SNP).
Results : There was no difference in blood pressure at any time point among the groups. There were no differences among groups in contractile responses to PE, U46619. The relaxant response to ACh and SNP did not differ among groups. The vasodilatory response to bradykinin (BK) was significantly attenuated in RX, and ERT improved this attenuation.
Conclusions : It was demonstrated that NO production through BK in endothelial cells was attenuated in mesenteric arteries by maternal protein restriction. ERT appears to improve endothelial dysfunction induced by maternal low protein diet.
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