BEHAVIORAL ASPECTS OF SALT INTAKE AND HYPERTENSION

这项研究是基于一个假设，即有一个敏感的 在发育早期， NaCl可以对参与控制的机制产生永久性影响， 钠和血压调节。 研究目的：（1） 进一步表征先前观察到的NaCl暴露变化，以及（2） 确定这些变化是否也伴随着 控制钠和血压调节的神经内分泌机制 在血压正常的Sprague-Dawley大鼠（S-DR）中， 高血压大鼠（SHR-S）、耐盐性自发性高血压大鼠（NaCl-Resistant Spontaneous Hypertension Rats （SHR-R）和NaCl抗性的Wistar-Kyoto大鼠（WKY）。 比较这些 四种菌株将提供一种评估它们之间相互作用的方法 早期氯化钠暴露与高血压的遗传易感性 成人 雌性大鼠将被喂食不同NaCl含量（0.12、1、3、0或8%）的饮食 氯化钠）在整个怀孕和哺乳期。 后代将继续 在产后30天内， 此后，所有动物 将维持在对照的1% NaCl饮食上，并作为成年人进行测试。 一 目的是确定早期NaCl暴露是否会改变 正常自由进食条件下和急性缺钠后， 给予呋塞米和48小时饮食钠剥夺。 将通过测量NaCl的变化来评估改变的味道机制 盐敏感性味觉神经元摄取和电生理反应 阿米洛利阻断NaCl味觉受体后，NaCl刺激。 到 确定早期氯化钠暴露是否导致排泄的主要障碍 或摄入量、血浆和尿电解质浓度以及血浆 血管紧张素II水平将根据饮食中的NaCl进行评估 缺乏和NaCl负荷。 第二个目标是确定早期 NaCl暴露导致NaCl摄入量和血压的长期变化 将根据颅内输注All或All- 受体拮抗剂在成年大鼠提出的低，中，高氯化钠 节食。 第三个目标是确定早期敏感性窗口， 氯化钠暴露。 早期饮食氯化钠暴露的影响，仅限于 产前、产后早期（0-14天）或断奶后早期（15- 16天）， 30)期间，对氯化钠摄入量和血压的成年大鼠将 评估。 最后一个目标是评估早期饮食氯化钠的影响， 暴露于NaCl摄入量，电解质排泄和血压之间 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.