DIETARY SALT AND BLOOD PRESSURE REGULATION

膳食盐和血压调节

• 批准号: 3349731
• 负责人: Silvia H Azar
• 金额: $ 18.5万
• 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/3349731
• 关键词: dietary mineral; disease /disorder model; embryo /fetus transplantation; environment associated hypertension; familial hypertension; laboratory rat; lactation; mother /embryo /fetus nutrition; newborn animals; nutrition related tag; spontaneous hypertensive rat; 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.

这些研究将调查遗传、母亲的影响 环境和母亲膳食盐过量对血压发展的影响 遗传性高血压大鼠的后代，假设： 易感成年人高血压的发展和严重程度 可以通过产前和产后早期的盐过量作用来改变 生活。 通过改变母体环境导致怀孕期间盐过量 加速子代高血压的宫内发育。 如果加盐 过量持续存在，哺乳期的母亲通过乳汁传播给后代， 通过胃肠道运输的因子， 与肾脏发育异常相结合会引起体液变化， 血压和肾脏导致进一步加速和/或加重 后代高血压。 断奶后，食盐摄入量等环境 与后代生命新阶段相关的因素调节 BP 发展到成熟的最后过程。 为了检验这个假设 我们将使用胚胎移植和交叉哺乳方法以及多元 分析。 自发性高血压大鼠（SHR）和对照组 将使用 Wistar-Kyoto 大鼠 (WKY)；环境因子为 NaC1 接受者母亲、护士和断奶婴儿的饮食中。 饮食含盐量 （低 0.3% 或 4% 盐饮食后给予并维持在指定的时间内） 饮食直至分娩。 然后一个“环境”和一个“遗传” 将进行操纵。 每个母亲都会成为一名护士，她的饮食也会 随机分配到低盐组或高盐组（16 组）。 一半是男的 然后，每个品系的幼崽将被交叉哺乳（32 组）。 所有的小狗都会 在 19 天时断奶，幼犬的饮食随机分为高盐或低盐（64 组）。 母亲终点为：产前体重、血压、心脏 率（交配后第 15 天、18 天和 20 天）。 后代终点将是胎儿 （第 15、18 和 20 天）和哺乳期（第 0、7 和 19 天）血压、心率、 肾脏/体重比和肾脏形态发育。 断奶后 后代将在第 6、16 周、6、9、12 个月时进行血压测量。 微穿刺将用于测量子宫内和产后早期血压。 拟议的研究将有助于区分遗传、 发育过程中的母体环境和外在环境 为高血压的预防措施提供合理依据 高血压易发人群。