BEHAVIORAL ASPECTS OF SALT INTAKE AND HYPERTENSION

这项拟议的研究是基于一种假设，即存在一种敏感的 在发育早期，饮食的生理后果 氯化钠可以对参与控制的机制产生永久性的影响。 钠和血压调节。建议进行以下研究：(1) 进一步描述之前观察到的氯化钠暴露的变化，以及(2) 确定这些更改是否也伴随着 控制钠和血压调节的神经内分泌机制 正常血压SD大鼠(S-DR)对氯化钠自发敏感 高血压大鼠(SHR-S)、耐盐自发性高血压大鼠 (SHR-R)和耐盐Wistar-京都大鼠(WKY)。这两种产品的比较 四个菌株将提供一种方法来评估 早期接触氯化钠与高血压的遗传易感性。成虫 雌性大鼠饲喂食盐含量不同的日粮(0.12、1、3、或8% 在整个孕期和哺乳期。后代将继续下去 在产后30天之前，一直吃同样的氯化钠饮食。此后，所有的动物 将维持在1%的对照食盐饮食中，并作为成年人进行测试。一 目的是确定早期接触氯化钠是否会改变 正常自由喂养条件和急性钠缺乏症后 给予速尿和48小时的饮食钠剥夺。 改变的味觉机制将通过测量氯化钠的变化来评估 盐敏感味觉神经元的摄取和电生理反应 用阿米洛利阻断氯化钠味觉感受器后对氯化钠刺激的反应。至 确定早期接触氯化钠是否会导致原发的排泄物悬挂 或摄入量、血浆和尿液电解质浓度以及血浆 血管紧张素II水平将根据饮食中氯化钠的反应进行评估 缺盐和盐负荷。第二个目标是确定早期 氯化钠暴露导致氯化钠摄入量和血压的长期变化 会对所有或所有的颅内输液做出反应- 成年大鼠在低、中、高盐环境下的受体拮抗剂 节食。第三个目标是确定对早期的敏感性窗口 暴露在氯化钠中。早期膳食氯化钠暴露的影响，仅限于 产前、出生后早期(0-14天)或断奶后早期(15-14天) 30)期间，对成年大鼠摄取氯化钠后血压将 评估过了。最终目标是评估早期饮食氯化钠的影响。 接触氯化钠摄入量、电解质排泄和血压 SHR-S、SHR-R和WKY。

The proposed research is based on the hypothesis that there is a sensitive period early in development when the physiological consequences of dietary NaCl can produce permanent effects on mechanisms involved in the control of sodium and blood pressure regulation. Studies are proposed to: (1) characterize further previously observed changes in NaCl exposure, and (2) determine whether these changes are also accompanied by changes in neuroendocrine mechanisms that control sodium and blood pressure regulation in normotensive Sprague-Dawley rats (S-DR), NaCl-sensitive spontaneously hypertensive rats (SHR-S), NaCl-resistant spontaneously hypertensive rats (SHR-R), and NaCl-resistant Wistar-Kyoto rats (WKY). A comparison of these four strains will provide a means for assessing the interaction between early NaCl exposure and genetic susceptibility to hypertension. Adult female rats will be fed diets that vary in NaCl content (0.12, 1, 3, 0r 8% NaCl) throughout pregnancy nad lactation. The offspring will be continued on the same NaCl diet until 30 days postpartum. Thereafter, all animals will be maintained on a control 1% NaCl diet and tested as adults. One goal is to determine whether early NaCl exposure alters NaCl intake during normal free-feeding conditions and after acute sodium deficiency induced by furosemide administration and 48 hours of dietary sodium deprivation. Altered taste mechanisms will be assessed by measuring changes in NaCl intake and electrophysiological responses of salt-sensitive taste neurons to NaCl stimulation after NaCl-taste receptor blockade with amiloride. To determine whether early NaCl exposure leads to primary hangs in excretion or intake, plasma and urinary electrolyte concentration, and plasma angiotensin II levels will be assessed in response to dietary NaCl deficiency and NaCl loading. A second goal is to determine whether early NaCl exposure leads to long-term changes in NaCl intake and blood pressure will be measured in response to intracranial infusions of All or an All- receptor antagonist in adult rats raised on either low, mid, or high NaCl diets. A third goal is to determine the window of sensitivity to early NaCl exposure. The effects of early dietary NaCl exposure, restricted to either prenatal, early postnatal (day 0-14), or early postweaning (day 15- 30) periods, on NaCl intake nad blood pressure of adult rats will be assessed. A final goal is to assess the effects of early dietary NaCl exposure on NaCl intake, electrolyte excretion, and blood pressure among SHR-S, SHR-R, and WKY.