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首页> 外文期刊>The Journal of Physiology >Developmental programming of aortic and renal structure in offspring of rats fed fat-rich diets in pregnancy.
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Developmental programming of aortic and renal structure in offspring of rats fed fat-rich diets in pregnancy.

机译:妊娠期富含脂肪饮食的大鼠后代的主动脉和肾结构的发育程序。

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Evidence from human and animal studies suggests that maternal nutrition can induce developmental programming of adult hypertension in offspring. We have previously described a model of maternal dietary imbalance in Sprague-Dawley rats whereby administration of a maternal diet rich in animal lard programmes the development of increased blood pressure, insulin resistance, dyslipidaemia, obesity and mesenteric artery endothelial dysfunction in adult offspring. To further characterize the mechanism of hypertension in this model we have examined vascular and renal structure in adult offspring of Sprague-Dawley rats fed a control diet (OC) or lard-rich diet (OHF) during pregnancy and suckling followed by a control diet post-weaning. To gain further insight, we assessed aortic reactivity and elasticity in an organ bath preparation and renal renin and Na+,K+-ATPase activity. Plasma aldosterone concentration was also measured. Stereological examination of the aorta in OHF demonstrated reduced endothelial cell volume and smooth muscle cell number compared with OC. Adult OHF animals showed increased aortic stiffness and reduced endothelium-dependent relaxation. Renal stereology showed no differences in kidney weight, glomerular number or volume in OHF compared with OC, but renin and Na+,K+-ATPase activity were significantly reduced in OHF compared with controls. Programmed alterations to aortic structure and function are consistent with previous observations that exposure to maternal high fat diets produces systemic vascular changes in the offspring. Despite normal renal stereology, altered renal Na+,K+-ATPase and renin activity offers further insight into the mechanism underlying the increased blood pressure characteristic of this model.
机译:来自人类和动物研究的证据表明,母体营养可以诱导后代成年高血压的发育。先前我们已经描述了Sprague-Dawley大鼠的母体饮食失衡模型,通过该模型,给予富含动物猪油的母体饮食会导致成年后代血压升高,胰岛素抵抗,血脂异常,肥胖和肠系膜动脉内皮功能障碍的发展。为了进一步表征该模型中的高血压机制,我们检查了怀孕和哺乳后喂饲对照饮食(OC)或猪油丰富饮食(OHF)的Sprague-Dawley大鼠成年后代的血管和肾脏结构-断奶。为了获得进一步的见解,我们评估了器官浴制剂中的主动脉反应性和弹性以及肾素和Na +,K + -ATPase活性。还测量血浆醛固酮浓度。在OHF中对主动脉进行的体视学检查显示,与OC相比,内皮细胞体积和平滑肌细胞数量减少。成年OHF动物表现出增加的主动脉僵硬度和减少的内皮依赖性舒张功能。肾脏立体显示,与OC相比,OHF的肾脏重量,肾小球数量或体积无差异,但与对照组相比,OHF中的肾素和Na +,K + -ATPase活性明显降低。对主动脉结构和功能的程序性改变与以前的观察结果一致,即母体高脂饮食会引起后代的全身血管变化。尽管肾脏立体学正常,但肾脏Na +,K + -ATPase和肾素活性的改变仍可进一步了解该模型血压升高的潜在机制。

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