DIETARY SALT AND BLOOD PRESSURE REGULATION

膳食盐和血压调节

• 批准号: 3349726
• 负责人: Silvia H Azar
• 金额: $ 16.22万
• 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/3349726
• 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.

这些研究将调查遗传学、母体 环境和母体膳食盐过量对BP发展的影响 遗传性高血压大鼠的后代，假设： 易感成年个体高血压的发展和严重程度 在产前和产后早期， 生活 通过改变母体环境导致妊娠期盐过量 加速了后代高血压在子宫内的发展。 盐若 过量的持续存在，哺乳期的母亲通过乳汁传递给后代， 通过胃肠道转运的因子， 与异常肾发育的结合引起体液的变化， 血压和肾脏导致进一步加速和/或加重 后代高血压 断奶后，盐的摄入量和其他环境 与后代新的生命阶段有关的因素调节了 BP发展到成熟的最后阶段。 为了验证这一假设 我们将使用胚胎移植和交叉哺乳的方法， 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NaCl 1 在受体母亲、保育员和断奶仔猪的饮食中。 饮食盐含量 (low 0.3%或4%的盐饮食后，并保持在其指定的 直到分娩。 一个是"环境"，一个是"遗传" 操纵将被完成。 每个母亲都将是一名护士，她的饮食将 随机分配到低盐或高盐组（16组）。 一半的男性 然后将每种品系的幼仔交叉哺乳（32组）。 所有的幼崽都会 在19天断奶，幼犬的饮食随机分为高盐或低盐（64 组）。 母体终点为：产前体重; t、BP、心脏 率（交配后第15、18和20天）。 后代终点为胎儿 (days 15、18和20）和哺乳期（第0、7和19天）BP、心率， 肾/体重比和形态学肾发育。 断奶后 后代将在6、16周、6、9、12个月时测量血压。 微穿刺将用于测量子宫内和产后早期BP。 拟议的研究将允许区分遗传， 发展中的母体环境和外部环境 高血压，这将提供一个合理的预防措施， 容易患高血压的人。