FAT & HYPERTENSION

胖的

• 批准号: 3356181
• 负责人: RUBEN D BUNAG
• 金额: $ 11.65万
• 依托单位: UNIVERSITY OF KANSAS MEDICAL CENTER
• 依托单位国家: 美国
• 财政年份: 1987
• 资助国家: 美国
• 起止时间: 1987-07-01 至 1992-04-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/3356181
• 关键词: afferent nerve; alloxan; antihypertensive agents; baroreceptors; blood flow measurement; caloric dietary content; cardiovascular disorder epidemiology; cardiovascular disorder prevention; computer data analysis; dietary lipid; dietary mineral; disease /disorder model; electrical potential; electrocardiography; experimental brain lesion; gender difference; genetic strain; heart rate; hemodynamics; hormone regulation /control mechanism; hyperinsulinism; hypertension; laboratory rat; longitudinal animal study; low salt diet; nutrient bioavailability; nutrition related tag; obesity; pathogenic diet; reducing diet; renin angiotensin system; spontaneous hypertensive rat; streptozotocin; sympathetic nervous system; ultrasound blood flow measurement; vascular resistance; vasoconstrictors; vasodilators; vasopressins

Studies are proposed to measure blood pressure chronically in different rat models of obesity and test the hypothesis that blood pressure becomes evaluated by changes in baroreflex sensitivity, cardiovascular reactivity, regional hemodynamics, or humoral regulation. Initial experiments will determine whether blood pressure becomes progressively elevated as rats gain weight following chemical or electrolytic lesions of the ventromedial hypothalamus, or prolonged feeding of high-fat and high-sugar diets, and compare the chronic time course of blood pressure changes with that occurring in Zucker "fatty' and Koletsky obese SHR rats. If hyperphagia occurs during induction of obesity in any of the models being studied, effects of diets containing reduced salt will be compared to determine how much of the change in blood pressure is due to salt loading. Subsequently, other experiments will study effects of dietary caloric restriction on blood pressure changes occurring in the various rat models in order to explore the possibility that reduction in body weight would alleviate hypertension as it does in man. Since hyperinsulinemia commonly occurs in all obese rat models, its contribution to the associated hypertension will be assessed by using subdiabetogenic doses of streptozotocin or alloxan to reduce pancreatic insulin secretion. If significant elevations of blood pressure are detected in obese rats, terminal experiments will be done to determine whether changes in baroreflex sensitivity, cardiovascular reactivity, or regional hemodynamics contribute to the ensuing hypertension. Finally, other terminal experiments will also assess the extent to which sympathetic, vasopressin, and renin-angiotensin pressor mechanisms participate in regulating blood pressure in obese rats. By obtaining basic information on what happens to blood pressure in obese rats, these studies may identify models that would allow detailed examination of mechanisms underlying obesity hypertension.

建议进行研究来长期测量血压， 不同的肥胖大鼠模型，并测试假设， 压力通过压力反射敏感性的变化来评估， 心血管反应性、局部血流动力学或体液 调控 最初的实验将确定血液是否 随着大鼠体重的增加，压力逐渐升高 在腹内侧的化学或电解损伤之后 下丘脑，或长期喂养高脂肪和高糖 饮食，并比较血压的慢性时间进程 Zucker“肥胖”和Koletsky肥胖中发生的变化 SHR大鼠。 如果在诱导肥胖期间发生摄食过多， 在所研究的模型中， 盐将进行比较，以确定有多少变化， 血压是由于盐负荷。 随后，其他 实验将研究饮食热量限制对 在各种大鼠模型中发生的血压变化 为了探索减轻体重的可能性， 会像人类一样缓解高血压。因为 高胰岛素血症通常发生在所有肥胖大鼠模型中，其 对相关高血压的贡献将通过 使用亚致糖尿病剂量的链脲佐菌素或四氧嘧啶， 胰腺胰岛素分泌。 如果血液浓度显著升高 压力检测肥胖大鼠，终端实验将 以确定压力反射敏感性的变化， 心血管反应性或局部血流动力学有助于 随之而来的高血压。 最后，其他终端实验 还将评估交感神经、加压素和 肾素-血管紧张素升压机制参与调节 肥胖大鼠的血压。 通过获取有关 肥胖大鼠的血压会发生什么变化，这些研究可能 确定能够详细审查 肥胖高血压的潜在机制。