DIETARY SALT AND BLOOD PRESSURE REGULATION

膳食盐和血压调节

• 批准号: 3349729
• 负责人: Silvia H Azar
• 金额: $ 17.91万
• 依托单位: UNIVERSITY OF MINNESOTA
• 依托单位国家: 美国
• 财政年份: 1985
• 资助国家: 美国
• 起止时间: 1985-09-30 至 1990-09-29
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/3349729
• 关键词: dietary mineral; disease /disorder model; embryo /fetus transplantation; environment associated hypertension; familial hypertension; lactation; mother /embryo /fetus nutrition; newborn animals; nutrition related tag; weanling animal

These studies will investigate the effects of genetics, maternal environment and maternal dietary salt excess, on BP development in offspring of genetically hypertensive rats, postulating that: the development and severity of hypertension in a susceptible adult individual could be modified by salt excess acting during prenatal and early postnatal life. Salt excess during pregnancy by altering maternal environment accelerates the in-utero development of offspring hypertension. If salt excess persists, the lactating mother transmits to the offspring, via milk, a factor(s) transported through the gastrointestinal tract which in combination to abnormal renal development induces changes in body fluids, BP, and the kidney leading to further acceleration and or aggravation of offspring hypertension. After weaning, salt intake and other environmental factors associated with the offspring's new stages of life modulate the final course of BP development through maturity. To test this hypothesis we will use an embryo transfer and cross-suckling approach and multivariate analysis. The spontaneously hypertensive rat (SHR) and the control Wistar-Kyoto rat (WKY) will be used; the environmental factor will be NaC1 in the diet of recipient mother, nurse and weanling. The diet salt content (low 0.3% or 4% salt diets given after and maintained on their assigned diets until delivery. Then one "environmental" and one "genetic" manipulation will be done. Each mother will be a nurse and her diet will be randomly assigned to either low or high salt (16 groups). Half the male pups of each strain will then be cross-suckled (32 groups). All pups will be weaned at 19 days, and the pup's diet randomized to high or low salt (64 groups). Maternal endpoints will be: pre-natal body weigh;t, BP, heart rate (days 15, 18, and 20 post-mating). Offspring endpoints will be fetal (days 15, 18 and 20) and suckling (days 0, 7 and 19) BP, heart rate, kidney/body weight ratio and morphologic renal development. Post-weaned offspring will have BP measurements at 6, 16 weeks, 6, 9, 12 months. Micropuncture will be used to measure in-utero and early post-natal BP. The proposed studies will allow to differentiate the role of genetic, maternal environment and extrinsic environment in the development of hypertension, which will provide a rational for preventative measures in the hypertension prone individual.

这些研究将研究遗传学，母体的影响 环境和孕妇饮食盐过量，在BP开发中 遗传性高血压大鼠的后代，假设： 易感成年人的高血压发展和严重程度 可以通过产前和早期产后早期的盐过量作用来改变 生活。 通过改变产妇环境，怀孕期间盐过量 加速了后代高血压的内在发育。 如果盐 多余的母亲持续存在，通过牛奶向后代传播 通过胃肠道运输的因素 肾脏发育异常的结合会导致体液的变化， BP，以及导致进一步加速和或加重的肾脏 后代高血压。 断奶后，盐摄入量和其他环境 与后代的新阶段相关的因素调节 BP发展的最终过程。 检验这一假设 我们将使用胚胎转移和交叉弹药方法和多元 分析。 自发性高血压大鼠（SHR）和对照 将使用Wistar-Kyoto Rat（WKY）；环境因素将是NAC1 在接受者母亲，护士和断奶的饮食中。 饮食盐含量 （低于0.3％或4％的盐饮食，并在分配的 饮食直到分娩。 然后是一个“环境”和一个“遗传” 操纵将完成。 每个母亲将是一名护士，她的饮食会 被随机分配给低盐或高盐（16组）。 一半的男性 然后，每种菌株的幼崽将被挤为（32组）。 所有幼犬都会 在19天后断奶，幼犬的饮食随机分配到高盐或低盐（64 组）。 产妇的终点将是：产前体重； t，bp，心脏 费率（第15、18和20天）。 后代终点将是胎儿 （第15、18和20天）和哺乳（第0、7和19天）BP，心率， 肾脏/体重比和形态肾脏发育。 断奶 后代将在6、16周，6、9、12个月时进行BP测量。 微型函数将用于测量utero内和早期产后BP。 拟议的研究将允许区分遗传的作用 孕产妇环境和外在环境的发展 高血压，这将为预防措施提供合理 容易发生的高血压。