AROUSAL OF A SPECIFIC AND PERSISTENT SODIUM APPETITE IN THE RAT WITH CONTINUOUS INTRACEREBROVENTRICULAR INFUSION OF ANGIOTENSIN-II
AROUSAL OF A SPECIFIC AND PERSISTENT SODIUM APPETITE IN THE RAT WITH CONTINUOUS INTRACEREBROVENTRICULAR INFUSION OF ANGIOTENSIN-II
复制标题
DOI：
10.1113/jphysiol.1980.sp013211
复制
发表时间：
1980-01-01
影响因子：
5.5
通讯作者：
FLUHARTY, SJ
中科院分区：
文献类型：
--
作者：
BRYANT, RW;EPSTEIN, AN;FLUHARTY, SJ
正常钠充足大鼠的大脑长时间暴露于血管紧张素II会产生显着且持续的钠食欲。短期、重复全身注射异丙肾上腺素或肾素（两者都会提高循环血管紧张素水平），以及重复颅内注射血管紧张素 II 会引起 2.7% NaCl 摄入量的增加。在第二个系列的实验中，将血管紧张素 II 直接连续输注到大脑中会引起大量的 3% 氯化钠摄入。除了大量摄入高渗氯化钠外，一些大鼠每天饮用的水量超过了其体重。动物不仅在连续输注血管紧张素 II 期间饮用大量 3% 氯化钠，而且在输注结束后，它们继续以与肾上腺切除大鼠相当的速度摄入氯化钠。大多数动物的持续性氯化钠摄入量在几天内减少，但其他动物在测量其摄入量期间（最多 7 个月）就继续饮用氯化钠。血管紧张素II连续输注的反应是剂量依赖性的。在 6 ng/h 至 6000 ng/h 的剂量范围内，水和 3% NaCl 的摄入量均有所增加。在相同的剂量范围内，钠食欲的持续性也呈剂量依赖性。血管紧张素诱导的盐食欲对钠是特异性的。动物不饮用 0.5 M-NH4Cl，仅在连续输注期间偶尔饮用少量 0.5 M-KCl。水的大量周转并不是钠食欲的原因。仅在输注血管紧张素期间给予大鼠大量饮用3% NaCl。未输液但给予糖精水以增加水摄入量的动物即使液体摄入量较高，也不会同时饮用3% NaCl。未接受颅内输注但胃内输注等于或超过血管紧张素输注期间饮用量的水的大鼠没有喝3% NaCl，但喝了一些水。开始输注血管紧张素后开始饮酒的情况因动物而异。氯化钠的饮用量与水的摄入量没有时间联系，尽管偶尔会观察到这种情况。尽管在整个夜间持续注入血管紧张素，但大部分饮酒发生在夜间。血管紧张素水平升高，可能与其他因素（例如醛固酮或促肾上腺皮质激素水平升高）一起导致钠食欲。荷尔蒙的变化可能会改变动物对盐的感知，使其更容易被接受。通过尚未了解的方式，在血管紧张素输注终止后，盐的可接受性持续增加。
Prolonged exposure of the brain of the normal Na-replete rat to angiotensin II produced a marked and persistent Na appetite. Short-term, repeated systemic injections of isoprenaline or renin (both of which raise circulating angiotensin levels), and repeated intracranial injections of angiotensin II evoked increased ingestion of 2.7% NaCl. In a 2nd series of experiments, continuous infusions of angiotensin II directly into the brain evoked extremely large intakes of 3% NaCl. In addition to large intakes of hypertonic NaCl some rats drank daily volumes of water that exceeded their body weight. Not only did the animals drink large volumes of 3% NaCl during continuous angiotensin II infusion, but after termination of the infusion they continued to ingest NaCl at a rate comparable to that of the adrenalectomized rat. In most of the animals the persistent NaCl intake diminished over several days, but other animals continued to drink NaCl for as long as their intake was measured (up to 7 mo.). The response to continuous infusion infusion of angiotensin II was dose-dependent. Both water and 3% NaCl intake increased over a dose range of 6 ng/h to 6000 ng/h. The persistence of the Na appetite was also dose-dependent across the same range of doses. Angiotensin-induced salt appetite is specific for Na. Animals did not drink 0.5 M-NH4Cl and only occasionally drank minimal amounts of 0.5 M-KCl during continuous infusion. The large water turnover was not responsible for the Na appetite. Rats given access to 3% NaCl only during infusion of angiotensin drank copiously. Animals that were not infused but were given saccharine-flavored water to increase their water intakes did not drink 3% NaCl offered at the same time even though fluid intake was high. Rats that did not receive intracranial infusions but were infused intragastrically with volumes of water equal to or exceeding the amounts that were drunk during angiotension infusion did not drink the 3% NaCl but did drink some water. The onset of drinking after the start of angiotensin infusion varied from animal to animal. NaCl drinking was not temporally linked to water intake, although this was observed occasionally. Most of the drinking occurred during the night although angiotensin was infused continuously throughout the nychthemeron. Increases in angiotensin levels, probably with other factors such as increased levels of aldosterone or ACTH, result in Na appetite. The hormonal changes may alter the animals'' preception of salt making it more acceptable. By means that are not yet understood the increased acceptability of salt persists after the termination of angiotensin infusion.