NEUROLOGICAL BASES OF FEEDING AND DRINKING

小剂量全身性盐皮质激素（DOCA或醛固酮）联合 将低剂量的血管紧张素II注入脑室 高钠大鼠诱导快速，可靠和强劲的食欲， 盐，并且钠耗尽大鼠的盐食欲被抑制， 用药物干扰血管紧张素II的大脑作用， 阻止其合成或阻断其受体。 这些发现支持 假设过量的钠摄入是由以下因素的协同作用引起的： 大脑中的两种激素肾钠保护-血管紧张素II (Ang II）和醛固酮（ALDO）。 内源性Ang I、Ang II和ALDO将通过放射免疫测定来测量， 钠缺乏，肾上腺切除，药物或激素治疗 直接评估假设。 合成阻断 内源性血管紧张素II与口服自我给药的卡托普利（施贵宝）将 测试的想法，在肾上腺切除大鼠，其中血管紧张素必须 在没有醛固酮的情况下，对盐的食欲完全依赖于 血管紧张素。 内源性ALDO的作用将在完整的 通过改变饮食中的盐含量和使用新的 盐皮质激素受体阻滞剂（RU 28318）是有效的和具体的。 肾素-血管紧张素系统存在于外周和脑中。 通过与ALDO的协同作用，它们唤醒盐食欲的效力将是 通过对比静脉输注Ang II或 竞争性的血管紧张素II拮抗剂与那些已经获得的 颅内灌注相同的药剂。 此外，神经系统 可能介导激素协同作用的机制将是 研究重点放在室周器官，以及影响 协同治疗及其产生的过量盐摄入量 老鼠的血压 食欲的个体发育将在 新生大鼠，其繁殖将在鸽子中进行研究。 过量的盐摄入与高血压病的病因有关。 了解其激素原因可能会导致合理的化学 治疗和减少盐摄入量的风险， 高血压

Small doses of systemic mineralocorticoid (DOCA or aldosterone) combined with infusions of low doses of angiotensin II into the cerebral ventricles of the sodium replete rat induce a rapid, reliable, and robust appetite for salt, and the salt appetite of the sodium deplete rat is suppressed by interference with the cerebral actions of angiotensin II with drugs that prevent its synthesis or block its receptors. These findings support the hypothesis that excess sodium intake is provoked by a synergy of action in the brain of the two hormones of renal sodium conservation - angiotensin II (Ang II) and aldosterone (ALDO). Endogenous Ang I, Ang II, and ALDO will be measured by radioimmune assay in the sodium deficient, the adrenalectomized, and the drug or hormone treated rat to evaluate the hypothesis directly. Blockade of synthesis of endogenous Ang II with orally self-administered captopril (Squibb) will test the idea that in the adrenalectomized rat, in which angiotensin must act without aldosterone, the appetite for salt is completely dependent on angiotensin. The role of endogenous ALDO will be evaluated in the intact rat by varying the salt content of its diet and by using a new mineralocorticoid receptor blocker (RU 28318) that is potent and specific. Renin-angiotensin systems exist both in the periphery and in the brain. Their potencies for arousal of salt appetite by synergy with ALDO will be compared by contrasting the results of intravenous infusion of Ang II or of competitive antagonists of Ang II with those already obtained with intracranial infusion of the same agents. In addition, the neurological mechanisms that may mediate the synergistic effect of the hormones will be studied with emphasis on the circumventricular organs, as will the effects of the synergy treatment and the excess salt intake that it produces on the rat's blood pressure. The ontogeny of the appetite will be studied in newborn rats, and its phylogeny will be studied in the pigeon. Excess salt intake is implicated in the etiology of hypertensive disease. An understanding of its hormonal causes could lead to rational chemical therapies and to reductions of salt intake in humans at risk for hypertension.